COLUMBIA  LIBRARIES  OFFSjTE 

HEALTH  SCIENCES  STANDARD 


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THE  DIAGNOSIS  AND  TREATMENT  OF 
HEART  DISEASE    . 


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DIAGNOSIS    AND    TREATMENT 

OF 

HEART    DISEASE 

PRACTICAL  POINTS  FOR  STUDENTS  AND 
PRACTITIONERS 


BY 


E.    M.    BROCKBANK 


M.D.  (Vict.),  F.R.C.P. 

HON.    PHYSICIAN,    ROYAL   INFIKMARY,    MANCHESTKR 
CLINICAL    LECTURER    ON    DISEASES    OF    THE    HEART,    DEAN    OF    CLINICAL    INSTRUCTION, 
«  UNIVERSITY    OF    MANCHESTEK 


SECOND  EDITION 
WITH  ILLUSTRATIONS 


PAUL  B.   HOEBER 

67-69   EAST  FIFTY-NINTH   STREET 

NEW  YORK 

1916 


[Printed  in  England] 


PREFACE  TO  SECOND  EDITION 

The  demand  for  a  second  edition  of  this  small  work  has 
enabled  me  to  alter  and  add  to  it  considerably.  I  hope 
it  will  prove  even  more  useful  now  to  students  and 
practitioners  than  it  did  in  its  original  form.  It  could 
have  been  improved  further  had  not  National  affairs 
distracted  attention  from  teaching  matters. 

E.  M.  B. 


PREFACE  TO  FIRST  EDITION 

(Entitled  "  Heart  Sounds  and  Murmurs,  Their 
Causation  and  Differentiation.") 

In  this  small  work  I  have  attempted  to  put  simply, 
clearly  and  in  convenient  pocket-book  form  for  clinical 
reference  the  elements  of  cardiac  auscultation  for  the 
use  of  students.  I  have  repeated  myself  a  good  deal 
with  the  object  of  making  an  argument  or  explanation 
as  complete  as  possible  in  the  one  place  and  thereby  of 
avoiding  turning  backwards  and  forwards. 

E.  M.  B. 
Manchester,  1911. 


CONTENTS 

SKCTION  PAOE 

1.    PRI  LIMINARY    CONSIDERATIONS  -  -  -  1 

Anatomy  and  Physiology. 

II.    K'uUTiNE  Examination  -  -  -  -        6 

What  patients  complain  of — The  arterial  pulse  : 
how  to  feel  it :  varieties :  tension :  wall  of 
artery — Venous  pulse — Inspection  of  patient : 
general  :  the  neck :  the  praecordia — Palpation  : 
cardiac  impulse  and  apex- beat — Percussion  : 
routine  method  :  cardiac  dulness — Auscultation. 

III.  The  Heart  Sounds      -  -  -  -      29 

The  first  sound  and  its  variations— The  second 
sound  and  its  variations — Rhythm  of  sounds: 
tic-tac  rhythm :  cantering  rhythm,  bruit  de 
galop. 

IV.  Heart  Murmurs  -  -  -  -      48 

Timing  —  Changes  in  the  valves  which  lead 
to  murmurs  :  obstruction  :  incompetence  — 
Physical  causes  :  fluid  veins  :  vibration  of  cur- 
tains: blood  changes,  hsemic  murmurs — Changes 
in  the  different  valves  which  cause  murmurs : 
auriculo-ventricular  valves,  stenosis,  dilatation, 
ulceration :  semilunar  valves — Crescendo  mur- 
mur— Murmurs  with  heart  sounds— Absence  of 
heart  sounds  with  normal  valves— Influence  of 
mobility  of  curtains  on  sounds, 

V.  Aheas  of  Audibility  of  Heart  Murmurs    -      65 

Situation   of   valves — Influence   of    change   of 
position  on  murmurs. 

VI.   Conduction  and  Transmission  of  Murmurs      68 

Conduction — Transmission, 
vii 


Vill  CONTENTS 

SECTION  PAOE 

VII.   Special  Characteristics  of  the  Different 

Valvular  Murmurs  -  -  -      72 

Mitral  murmurs — Rheumatism  in  childhood  : 
nodules — Crescendo  murmur — Tricuspid  mur- 
murs— Aortic  murmurs — Posture  murmur — 
Pulmonary  murmurs. 

VIII.   H.EMic  Murmurs  -  -  -  -      89 

Cardiac — Vascular:  bruit  de  diable. 

IX.   Exocardial  Sounds     -  -  -  -      91 

Pericardial — Cardio-respiratory. 

X.   Septic   Endocarditis,   Pericarditis,   Angina 

Pectoris       -  -  -  -  -      93 

Septic,  malignant,  or  ulcerative  endocarditis — 
Pericarditis,  simple,  serous,  purulent — Adherent 
pericardium — Angina  pectoris. 

XL   Cardiac  Irregularity  resulting  from  Dis- 
turbances OF  Stimulation  -  -      98 

Electrocardiogram  —  Tachycardia  :  apprehen- 
sive heart  :  paroxysmal  tachycardia  —  Slow 
pulse  :  bradycardia  —Heart-block — Irregular  or 
intermittent  pulse  :  premature  systole,  extra- 
systole — Sinus  arrhythmia — Auricular  fibrilla- 
tion— Auricular  flutter. 

XII.   Treatment  of  Cardiac  Disease         -  -     107 

Before  muscle  failure  :  general :  diet :  exercise  : 
drugs — Cardiac  muscle  failure  :  rest  in  bed  : 
diet  :  sleep  :  drugs — Drugs  acting  on  the  heart 
muscle  :  digitalis  :  strophanthus  :  cafifein  : 
strychnine  -  Vessel  dilators  —  Treatment  of 
special  forms  of  heart  disease :  mitral  valve : 
aortic  valve :  alcoholic  heart  failure :  angina 
pectoris. 

Index     -  -  -  -  -  -     118 


PRACTICAL  POINTS  IN  THE 

DIAGNOSIS   AND   TREATMENT  OF 

HEART  DISEASE 


PRELIMINARY  CONSIDERATIONS 

AXATOMY   AND    PHYSIOLOGY. 

Anatomy. — The  heart  is  a  conical-shaped  organ  with 
the  great  vessels  attached  to  its  base ;  it  is  about  the 
size  of  its  owner^s  clenched  fist,  and  lies  obliquely  in 
the  thorax,  inclined  from  above  downwards,  forwards, 
and  to  the  left,  with  one-third  (the  base)  to  the  right 
and  two-thirds  to  the  left  of  the  mid-sternal  line. 

The  anterior  aspect  of  the  heart  is  formed  almost 
entirely  by  the  right  ventricle,  right  auricle,  and  infun- 
dibulum  or  conus  arteriosus ;  only  a  suiall  part  of  it, 
namely,  the  apex  and  about  half  an  inch  along  its  left 
margin,  is  formed  by  the  left  ventricle.  The  tip  of  the 
left  auricle  just  comes  to  the  surface  behind  the  second 
interspace.  It  is  covered  by  lung  all  over  except  in 
the  mid-sternal  line,  and  a  triangular  space  formed  by 
the  mid-sternal  line,  a  line  from  the  fourth  chondro- 
sternal  articulation  to  the  junction  of  the  fifth  costal 
cartilage  with  its  rib,  and  the  line  of  liver  dulness,  the  so- 
called  area  of  superficial  cardiac  dulness  (see  p.  26). 

1 


^  HEAUT   DISEASE 

Surface  anatomy. — The  upper  limit  is  behind  the 
second  costal  cartilage.  Its  right  side  extends  half  an 
inch  beyond  the  right  edge  of  sternum.  Its  apex  or  its 
limit  to  the  left  is  in  the  fifth  intercostal  space  two  and  a 
half  inches  beyond  the  left  edge  of  the  sternum ;  in  adult 
males  this  is  about  one  inch  below  and  three-quarters 
of  an  inch  to  the  sternal  side  of  the  nipple.  Its  lower 
limit  is  about  the  sixth  rib,  where  the  heart  lies  in  con* 


Fig.  1. 

A.,  Aorta  ;  A.V.,  aoriic  valve  ;  i»/.,  mitral  valve  ;  P. A.,  pulmonary  artery  ;  /'.  V.,  pul- 
monary valve  ;  li.A,,  right  auricle  ;  &  F.,  septum  ventriculorum  ;  S.  F.C.,  superior 
vena  cava;  T.r.,  tricuspid  vrlve.    (Cunningham.) 

tact  with  the  diaphragm.     In  children  the  heart  may  be 
rather  higher  and  its  apex  farther  out  in  the  chest. 

N.B. — The  ni'pi)le  in  men,  normally  situated  ahoni 
4  inches  from  the  mid-sternal  line,  may  be  nearer  than 
this  to  the  sternum  if  the  chest  is  not  well  developed. 
An  apex-beat  outside  the  vertical  nipple  line,  therefore, 
need  not  necessarily  indicate  disease.     In  children  the 


ANATOMY  3 

apex-beat  may  be  farther  out  and  up  in  relation  to  the 
nipple  than  it  is  in  man.  The  nij^ple  in  women  is  use- 
less as  a  point  which  has  definite  position. 

The  surface  lines  or  landmarks  which  are  of  use  in 
the  examination  and  note-taking  of  thoracic  affections 
are  : 

The  mid- sternal  line  down  the  middle  of  the  sternum. 

The  lateral  sternal  lines  down  the  right  and  left  edges 
of  the  sternum. 

The  parasternal  lines  midway  between  the  lateral 
sternal  lines  and 

The  mid-clavicular  lines,  which  are  lines  drawn  per- 
pendicularly from  the  middle  of  the  collar-bones  or 
midway  between  the  middle  of  the  suprasternal  notch 
and  the  top  of  the  acromion. 

The  nijpjple  line  in  the  normal  adult  male  is  practically 
the  same  as  the  mid-clavicular  line,  the  nipple  being 
situated  about  four  inches  from  the  mid-sternal  line. 

The  axillary  lines,  anterior,  mid,  and  posterior,  running 
perpendicularly  downwards  through  the  anterior,  mid, 
and  posterior  regions  of  the  axilla. 

The  scaptdar  lines,  through  the  angles  of  the  scapulas. 

Nervous  mechanism  of  the  heart-beat.— The  stimu- 
lation of  the  heart  for  its  beating  is  carried  on  by 
means  of  a  special  form  of  tissue,  partly  nervous  and 
partly  heart  muscle  in  structure,  which  occurs  in  aggre- 
gations or  nodes,  and  connecting  or  end  fibres. 

(1)  The  sino-auricular  node  is  in  the  subepicardial 
tissue  at  the  junction  of  the  superior  vena  cava  and  the 
right  auricular  appendix.  This  node  is  the  most  highly 
developed  aggregation  of  the  neurQ-muscular  tissue,  and 
it  initiates  the  stimulus  and  sets  the  pace  and  rhythm  of 


4  HEART   DISEASE 

the  heart.  It  is  believed  to  receive  fibres  from  the  vagus 
and  sympathetic  nerves.  From  it  the  stimulus  passes, 
in  some  way  not  fully  understood,  through 


S.A.  node 


A .  V.  node 
A  V.  bundle 


Fig.  2. — The  Cardiac  Nervous  Mechanism. 

S.A.  node,   Siuo-auricular  node;    A.V.   node,   aiiriculo-ventricalar  node  (Tawaia) 
A.V.    bundle,  auriculo-ventricular  bundle.      The  connection  between  the   S.A. 
node  and   the   A.V.    node  is   indefinite.       It  may  be  through  the  contracting 
auricular  niu.scle. 

(2)  The  auricular  walls  to  the  aiiriculo- ventricular  node, 
which  lies  m  the  right  side  of  the  auricular  septum. 
From  this  a.v.  node  the  stimulus  is  carried  by 

(3)  Hie  auriculo-ventricular  hundle  {a.v.  bundle)  to  the 
ventricles.     This   bundle  divides  in  the   interventricular 


NERVOUS   MECHANISM  O 

septum  into  two  branches^  which  ultimately  spread  out 
in  the  subendocai'dial  tissue  of  right  and  left  ventricles 
as  Purkinje's  fibres.  The  papillary  muscles  are  said  to 
be  the  first  part  of  the  ventricles  to  receive  the  stimulus 
to  contract. 

It  is  not  known  how  the  stimulus  from  the  sino-auri- 
cular  node  traverses  the  auricles.  It  is  probably  carried 
by  the  muscle  fibres^  regular  and  complete  contraction 
of  which  is  essential  for  the  regular  contraction  of  the 
ventricles.  At  any  rate,  irregular  and  incomplete  con- 
traction of  the  auricles  results  in  irregular  contraction 
of  the  ventricles.  In  a  marked  condition  of  auricular 
disease,  in  which  the  wall  is  dilated,  and  in  which  the 
muscle  is  in  a  state  of  over-excitability  and  is  making 
constant  incomplete  attempts  to  contract  (see  Auricular 
fibrillation  and  Flutter),  there  is  an  extreme  degree  of 
irregularity  in  the  ventricular  rhythm. 

Whilst  the  stimulus  for  the  heart  beat  arises  normally 
in  the  sino  auricular  node,  and  is  rhythmic  or  regular  in 
origin,  in  abnormal  conditions,  functional  or  organic,  it 
may  arise  in  other  parts  of  the  nervous  mechanism,  or 
be  arrhythmic  or  irregular  in  origin.  Thus  it  not  un- 
commonly starts  in  the  auricle  or  ventricle  causing  the 
condition  known  as  premature  systole  (q.v.),  or  pre- 
mature stimuli  may  leave  the  sino-auricular  node  A\dth 
the  same  result. 

If  the  nervous  tissue  of  the  heart  be  changed  struc- 
turally by  disease,  or  become  unduly  irritable,  irregu- 
larity in  the  action  of  the  heart  results,  giving  rise  to 
conditions  (i^. v.)  known  as  premature  systole,  heart-block, 
auricular  fibrillation,  and  paroxysmal  tachycardia. 


II 

ROUTINE   EXAMINATION 

What  Patients  with  Heart  Disease  complain  of. 

Patients  suffering  from  the  worst  forms  of  heart  disease 
may  feel  perfectly  well,  and  have  no  complaint  of  any  sort. 
Their  cardiac  weakness  may  only  be  discovered  during 
the  course  of  an  examination  for  life  insurance,  or  for 
some  illness  not  connected  with  the  heart.  As  a  rule, 
however,  they  do  complain  of  one  or  more  subjective 
symptoms,  chiefly  shortness  of  breath,  palpitation,  and 
pain. 

1.  Shortness  of  breath,  especially  after  only  slight 
exertion,  as  on  going  up  a  flight  of  household  stairs  or 
up  a  short  hill.  In  more  severe  conditions  the  patient 
may  be  awakened  from  his  sleep  with  a  sensation  of 
breathlessness  and  tumultuous  action  of  the  heart — a 
very  distressing  condition. 

2.  Palpitation,  or  unusual  action  of  the  heart,  which 
attracts  its  subject^s  attention.  The  quick  action  with 
a  "throbbing"  sensation  in  the  neck  resulting  from 
emotional  or  muscular  overaction  is  commonly  met  with, 
and  generally  described  as  palpitation.  It  may  be  met 
with  in  normal  as  well  as  diseased  hearts.  A  "  flutter- 
ing" or  "  tumbling"  sensation  is  often  felt.     This,  how- 


ROUTINE  EXAMINATION  ' 

ever,  in  its  slighter  forms  may  be  present  wlien  the  heart 
is  quite  sound,  and  be  due  to  functional  disturbance  of 
the  regular  stimulation  of  the  heart.  In  disease,  Avhen 
the  heart  is  enlarged  and  its  action  forcible,  this  symptom 
is  often  most  distressing*,  especially  when  it  wakens  the 
patient  up  out  of  his  sleep  with  a  smothering  feeling. 

3.  Pain  (1)  over  the  praecordia,  made  worse  by  exer- 
tion or  increased  quickness  of  beat,  is  met  with  chiefly  in 
cardiac  enlargement  due  to  valvular  disease  or  adherent 
pericardium.  There  is  much  tenderness  to  the  touch  in 
these  cases. 

Or  (2)  shooting  down  the  arms,  especially  the  left 
arm,  or  in  the  shoulder  or  up  the  neck,  in  aneurysm  or 
angina  pectoris.  There  is  oft^n  also  a  sense  of  suffoca- 
tion or  of  gripping  of  the  heart,  mth  apprehension  of 
impending  death,  in  anginal  cases  while  the  pain  is 
present. 

N^.B. — Pain  in  the  upper  arms,  especially  in  the  left 
arm  J  w  up  the  haclc  of  the  nech,  may  he  the  first  indication 
of  aneurysm  of  the  arch  of  the  aorta. 

The  Cause  of  the  Cardiac  Pain. — The  pain  is  one  form 
of  referred  pain.  The  heart,  developmentally,  is  asso- 
ciated with  the  first  eight  dorsal  segments  and  nerves, 
and  painful  impressions  arising  in  it  are  usually  referred 
to  the  first  and  second  dorsal  nerves.  The  cutaneous 
distribution  ^of  these  nerves  is  the  inner  aspect  of  the 
arm  as  far  down  as  the  elbow,  and  anginal  pains  which 
arise  from  disease  at  the  base  of  the  ventricles,  or  first 
part  of  the  arch  of  the  aorta,  are  referred  to  the  shoulder 
and  down  the  arm. 

HsemoPPhag'e  from  mucous  surfaces  may  be  com- 
plained of    by  patients  with  mitral   disease,  especially 


8  HEART   DISEASE 

mitral  stenosis.  Epistaxis,  haemoptysis,  haematemesis, 
and  bleeding  from  the  ears,  have  been  present  in  cases 
under  my  care.  The  heart  must  therefore  always  be 
carefully  examined  in  all  cases  of  mucous  membrane 
haemorrhages. 

Dropsy. — In  heart  disease  dropsy  affects  the  legs  in 
the  first  place,  and  is  improved  by  rest  in  bed.  In 
looking  for  oedema  pressure  should  be  applied  deliber- 
ately, for  about  five  seconds,  over  the  face  of  the  tibia 
near  the  ankle,  and  also  over  the  sacrum.  Slight  degrees 
of  it  will  be  overlooked  unless  this  care  be  taken. 

Coug^h  from  congestion  of  the  pulmonary  mucous 
membrane  is  a  frequent  consequence  of  disease  of  the 
mitral  or  tricuspid  valves. 

The  Arterial  Pulse. 

N.B. — The  pulse  should  be  examined  at  the  com- 
mencement of  the  investigation  of  any  heart  affection. 

Much  valuable  information  can  be  obtained  in  heart 
affections  by  an  intelligent  feeling  of  the  radial  pulse 
with  the  fingers.  The  sphygmograph  is  an.  interesting 
instrument,  and  gives  instructive  information  when  you 
know  the  kind  of  tracing  you  ought  to  get  and  the 
proper  way  to  get  it.  But  even  to  one  experienced  in 
its  use  it  gives  but  little  information  which  escapes  the 
practised  fingers. 

The  best  way  to  feel  the  radial  pulse  is  to  use  two 
hands  for  the  purpose.  One  hand  is  to  steady  the 
patient's  wrist,  by  holding  his  hand  so  as  to  allow  the 
delicate  application  of  three  fingers  of  the  other  hand 
to  the  artery,  as  it  runs  over  the  end  of  the  radius. 
The  thumb,  to  further  steady  matters,  should  be  placed 
behind  the  patient's  wrist.     All  three  fingers  should  be 


THE   PULSE  9 

placed  closely  together  over  the  end  of  the  radius,  so 
that  the  artery  can  be  pressed  against  it,  and  not  against 
the  less  resisting  soft  tissues.  The  index  finger  should 
be  applied  firmly  as  close  to  the  base  of  the  metacarpal 
bone  of  the  thumb  as  possible  to  obliterate  the  junction 
of  the  radial  artery  with  the  palmar  arch,  and  prevent 
any  wave  coming  round  that  way.  The  ring  finger  is 
used  to  tell  when  the  pulse  in  the  artery  is  beating  or 
not,  and  the  fourth  finger  to  apply  pressure  over  the 
artery  and  estimate  the  amount  of  force  necessary  to 
obliterate  the  pulse  in  the  radial  artery.  In  this  way 
changes  in  the  tension  of  the  bloodvessel  can  be  very 
accurately  estimated  witli  a  little  practice  and  knowledge 
of  the  normal  condition  of  aifairs. 

Another  useful  icay  of  feeling  the  jndse  is  to  grip  the 
lower  end  of  the  radius  between  the  forefinger  and 
thumb  of  one  hand,  with  the  finger  applied  firmly  over 
the  artery  close  up  to  the  base  of  the  metacarpal  bone 
of  the  thumb  to  cut  oif  the  palmar  arch  anastomosis 
pulse,  and  then  to  apply  the  first  and  second  fingers  of 
the  other  hand  to  the  radial  artery  as  before.  In  either 
method  all  three  fingers  must  occupy  as  little  space  as 
possible,  so  that  they  can  manipulate  the  artery  as  it 
runs  in  front  over  the  end  of  the  bone. 

It  is  sometimes  instructive  to  feel  the  pulse  by  gripping 
the  wrist  Avith  the  hand  in  such  a  way  that  the  palm  of 
the  observer  will  lie  over  both  radial  and  ulnar  arteries 
and  feel  their  pulsation,  at  the  same  time  elevating  the 
patient^s  forearm  so  that  there  is  a  considerable  stretch 
of  perpendicular  artery.  In  this  way  the  water-hammer 
or  Corrigan^s  pulse  is  best  developed,  both  arteries  slap- 
ping their  pulse  wave  against  the  palm  of  the  hand,  and 
its  simulation  by  a  low  tension  pulse  of  cardiac  dilata- 
tion reduced  to  a  minimum, 


10  HEART  DISEASE 

No  apology  need  be  made  for  giving  such  details  of 
good  methods  of  feeling  the  pulse,  for  by  their  adoption 
an  accurate  estimate  of  changes  in  the  pulse  tension 
may  be  more  easily  made,  and  variations  from  the 
normal  m  other  ways  more  easily  recognized  than  if  less 
deliberate  methods  be  adopted. 

Congenital  abnormalities  in  the  anatomy  of  the  radial 
arteries  may  occur,  and  must  be  allowed  for.  Thus  the 
radial  artery  may  be  of  smaller  size  than  normal  in  one 
or  both  wrists,  and  make  pulse-feeling  rather  difficult. 

Comparison  of  the  two  radial  arteries. — Inequality  in 
the  pulse  wave  of  the  two  radial  arteries  may  occur,  and 
be  due  to — 

1.  Congenital  causes. 

2.  Pressure  on  the  artery  somewhere  on  the  proximal 
side  of  the  wrist  (with  a  thoracic  aneurysm  or  new 
growth). 

3.  Changes  in  the  wall  of  the  artery  (atheroma). 

4.  Obstruction  in  the  lumen  of  the  vessel  (embolism 
or  thrombosis). 

The  points  to  bs  noticed  in  feeling  the  radial  pulse 

are,  the  rate,  volume,  regularity,  tension,  condition  of 
the  vessel  wall,  aud  the  comparison  between  the  two 
radial  pulses. 

Pulse-pate.  —  In  counting  a  pulse-rate,  it  is  to  be 
remembered  that  the  result  does  not  always  indicate 
the  rate  the  heart  is  beating  at.  It  generally  does, 
but  in  one  form  of  heart  disease — namely,  auricular 
fibrillation — in  which  the  rhythm  and  force  of  the 
ventricular  systole   is   extremely  irregular  and  uneven, 


THE  PULSE  11 

many  of  the  ventricular  beats,  which  are  considerably 
increased  in  number,  are  so  feeble  that  they  do  not 
transmit  a  pulse  wave  to  the  radial  artery.  Therefore, 
when  the  radial  pulse  is  irregular  in  rhythm  and  size  of 
wave,  and  increased  in  frequency  above  the  normal,  the 
stethoscope  should  be  applied  to  the  heart  whilst  the 
pulse  is  being-  counted. 

A  quick  pulse  in  heart  disease  practically  always 
means  either 

1.  Some  dehility  of  the  heart  muscle — that  is,  inability 
to  do  the  extra  work  thrown  on  it  by  the  abnormal 
condition  by  its  usual  number  of  beats.  It  often  means 
some  giving  way  of  the  heart  muscle,  that  is,  cardiac 
muscle  failure,  but  not  necessarily  so ;  or 

2.  An  abnormal  excitability  of  the  nervous  mechanism 
which  causes  an  abnormally  increased  number  of  stimuli 
sent  to  the  ventricles. 

These  points  will  be  referred  to  again  under  the 
headings  tachycardia  and  irregular  pulse. 

An  abnormally  slow  pulse  in  heart  disease — that  is,  a 
rate  below  50,  especially  one  below  30 — frequently  means 
some  pathological  change  in  the  auriculo-ventricular 
{a.-v.)  bundle,  which  impedes  the  conduction  of  stimuli 
from  the  auricular  nervous  mechanism.  (See  Brady- 
cardia.) In  this  case  the  auricles  will  be  contracting 
more  frequently  than  the  ventricles. 

A  certain  but  small  number  of  persons  have  a  heart- 
rate  below  50  with  auricles  contracting  as  slowly  as  the 
ventricles. 

The  volume  of  a  pulse,  that  is,  whether  it  is  large  and 
full  or  small  and  empty,  depends  chiefly  on  the  amount 
of  blood  propelled  by  the  ventricle  into  the  aorta  at  each 
systole. 


12  HEART  DISEASE 

Small  and  empty  pulses. — In  mitral  disease  the  pulse 
is  often  small  and  empty,  because  in  stenosis  less  than 
the  normal  amount  of  blood  enters  the  left  ventricle 
during  its  diastole,  and  in  incompetence  some  reguEgi- 
tates  into  the  auricle.  In  either  case  an  abnormally 
small  amount  passes  from  the  ventricle  into  the  aorta 
with  each  beat.  Furthermore,  when  the  ventricles  in 
mitral  disease  are  contracting  Avith  increased  rapidity, 
irregularity  in  rhythm,  and  inequality  in  force,  only  a 
considerably  reduced  amount  of  blood  has  time  to  pass 
into  the  left  ventricle  for  it  to  contract  on. 

With  marked  aortic  stenosis  the  pulse  is  a  small  one, 
and  there  is  delay  in  its  transmission  to  the  wrist. 

A  large  and  full  pulse  is  met  with  when  there  is  an 
abnormal  amount  of  blood  expelled  from  the  ventricle 
into  the  aorta,  and  this  is  met  with  in  cases  of  dilatation 
of  the  left  ventricle  with  hypertrophy.  In  dilatation 
without  adequate  compensation  the  pulse  often  lias  a 
soon-full,  soon-empty,  or  slapping  character,  which  may 
simulate  very  closely  a  Corrigan\s  or  water-hammer 
pulse  iq.v.). 

Reg'Ularity. — Normally  the  heart,  and  therefore  the 
pulse-beats,  follow  each  other  regularly  in  rhythm  and 
uniformly  in  character.  It  is  very  common,  however, 
to  meet  with  irregularity  in  rhythm  and  varying  character 
of  heart-beat  and  pulse-wave,  not  only  when  the  heart 
is  diseased,  but  also  when  it  is  quite  sound. 

In  healthy  children  the  heart  may  be  irregular,  its 
rate  varjnng  with  inspiration  and  expiration.  A  similar 
irregularity  in  rhythm  is  often  met  with  in  nervous 
people. 

The  commonest  form  of  irregularity  in  adult  life  is 
the  so-called  missed  beat,  in  which  a  heart-beat  and  a 


PULSE  TENSION  13 

pulse-wave  apparently  drop  out.  What  happens  is  that 
the  heart  gives  a  premature  and  weak  contraction^  which 
does  not  create  a  pulse-wave.  (See  Premature  or  extra 
systole.)  This  frequently  occurs  in  normal  hearts  as  the 
result  of  digestive  disturbances. 

The  other  extreme  is  met  with  in  certain  forms  of 
heart  disease  when  scarcely  two  successive  beats  of  the 
heart  and  pulse  are  regular  in  rate  or  uniform  in  char- 
acter. The  beats  occur  in  a  most  irregular  way  (delirium 
cordis),  and  with  more  or  less  greatly  increased  rapidity. 
Sometimes  the  pulse-rate  is  uncountably  fast.  (See 
Intermittent  pulse  and  Auricular  fibrillation.)  Between 
these  two  extremes  lie  varying  degrees  of  irregularity. 

Tension. — increased  tension  is  an  important  indica- 
tion of  pathological  processes  taking  place  in  the  system, 
the  most  important  of  which  are  arteriosclerosis  and 
interstitial  nephritis.  It  may  be  the  first  physical  sign 
of  these  diseases,  and  when  it  is  present  the  urine  must 
be  examined  carefully  by  boiling  and  acidulation — the 
most  delicate  test  for  albumen.  The  specific  gravity  of 
the  urine  will  probably  be  low,  and  often  only  a  very 
faint  trace  of  albumen  is  found,  or  none  at  all. 

Nocturnal  polyuria. — There  will,  however,  generally 
be  obtained  a  history  of  nocturnal  polyuria  as  well — 
that  is,  the  necessity  of  getting  up  regularly  at  night 
two  or  three  times  to  pass  a  considerable  amount  of 
urine.  In  making  this  point,  it  must  be  ascertained  how 
much  fluid  is  drunk  late  at  night,  for  many  men  take 
half  a  pint  at  least  of  nightcap  fluid,  such  as  whisky 
and  water,  hot  milk,  or  plain  hydropathic  hot  water; 
but  this  will  rouse  them  only  once  in  the  night  as  a  rule, 
and  generally  early  in  the  morning.  Further,  the  in- 
creased frequency  of  micturition  in  small  amounts  caused 


14  HEART  DISEASE 

by  an  irritating  prostate  must  not  be  confused  with  high 
tension  polyuria. 

Increased  tension  may  be  caused  by  absorption  of 
toxins  from  the  alimentary  canal  without  there  being 
any  primary  interstitial  nephritis.  This  condition  may 
last  for  years,  with  its  attendant  discomforts. 

In  mitral  stenosis  the  pulse,  though  small,  is  often  one 
of  considerable  high  tension. 

The  distinction  between  hardness  of  the  wall  of  the 
artery  and  increase  of  arterial  tension  must  be  borne  in 
mind.  Either  may  be  present  without  the  other,  or 
both  may  be  present  together. 

Abnormally  low  tension  is  rather  more  difficult  to 
make  out.  It  is  present  in  debilitated  states  in  children 
who  are  subject  to  fainting  attacks  with  no  definite 
ascertainable  cause. 

The  condition  of  the  wall  of  the  artery  must  be 
made  out  by  rolling  it  under  the  fingers  against  the 
end  of  the  i*adius.  When  this  is  done,  a  normal  artery 
can  scarcely  be  felt  at  all  after  the  pulse-wave  has  been 
obliterated,  whilst  a  diseased  one  feels  more  or  less  hard, 
like  w  piece  of  string  when  there  is  fibroid  degeneration 
of  the  middle  coat,  or  like  a  hard  calcareous  tube  (pipe- 
stem  artery)  with  marked  atheromatous  degeneration. 
Movements  of  the  fingers  in  the  long  axis  of  the  end 
of  the  radius  will  reveal  any  annular  deposits  of  cal- 
careous material. 

Venous  Pulse. 

The  venous  pulse  affords  valuable  information  in  heart 
disease,  especially  of  the  condition  of  the  right  side  of 
the  heart.  The  only  vein  in  which  it  can  be  observed  is 
the  jugular  vein,  between  the  tlioi*acic  attachments  of 


THE  VENOUS  PULSE 


15 


tlie  sterno-mastoid  muscle.  When  there  is  ohstructioR 
to  the  flow  of  blood  from  the  right  auricle  into  the 
ventricle,  the  jugular  veins  are  distended,  and  stand  out 


■r.  a. 


V.  V. 


R 


E.  C. 


P. 


Fig.  3. 

V.  a. ,  Auricular  form  of  venous  pulse 
V.  v.,  Ventricular  form  of  venous  pulse. 
R.,        Radial  pulse. 
£.  C,  Electrocardiogram. 

P. ,       Phonoscope  tracing  showing  heart  sounds  and  murmur 
a.,  Auricular  wave  ;    v.,  ventricular  wave  ;      c,  carotid  waves. 
I.  and  II.,  first  and  second  heart  sounds.      '1  second  intervals  of  time. 

prominently,  but    often  there  is  no   visible   distension, 
let  alone  pulsation,  of  the  veins. 

With  obstruction  to  the  large  veins  in  the  chest  there 
will  be  distension  of  the  veins  in  the  neck  but  no 
pulsation. 


16  HEART    DISEASE 

The  venous  pulse  cannot  be  felt  by  the  finger  like 
the  arterial  pnlse^  but  requires  a  special  recording  ap- 
paratus for  its  investigation.  For  the  use  of  this  clinical 
polygraph  considerable  experience  and  practice  is  neces- 
sary. Its  application  is  consequently  limited  to  hospital 
practice  or  to  the  work  of  a  few  specialists.  Whilst  it 
gives  information  which  helps  in  the  understanding  of 
the  conditions  present  in  heart  disease,  especially  con- 
cerning' the  condition  of  the  auricles  and  the  relative 
number  of  auricular  and  ventricular  contractions,  it 
does  not  as  often  afford  much  assistance  in  treatment 
beyond  that  gained  by  other  and  more  manifest  evidence 
of  cardiac  muscle  failure. 

Jugular  pulse  waves. — The  common  form  of  jugular 
pulse  tracing  is  known  as  the  auricular  form,  and  shows 
three  waves.  The  first,  or  the  auricular  (a.)  wave,  is 
caused  by  auricular  systole;  the  next  and  smaller  wave 
is  called  the  carotid  (c.)  wave,  and  is  probably  caused 
by  the  pulse-wave  in  the  carotid  artery  being  trans- 
mitted through  the  jugular  vein  to  the  surface  ;  and  the 
last,  or  ventricular  (?;.)  wave,  is  caused  by  the  rebound 
of  blood  in  the  filling  auricle  against  the  closed  tricuspid 
valve  (Fig.  3,  V.  a). 

In  the  other  form  of  venous  pulse,  known  as  the  ven- 
tricular venous  pulse,  there  is  no  a.  wave,  the  v.  wave 
predominating.  In  this  case  there  is  no  contraction  of 
the  auricle,  this  organ  being  paralyzed  and  acting 
merely  as  a  reservoir  (Fig.  3,  V.  v). 

The  jugular  pulse,  then,  gives  information  as  to  what 
is  going  on  in  the  right  side  of -the  heart  chiefly.  It  is 
recorded  synchronously  on  paper  by  means  of  a  poly- 
graph with  the  radial  pulse,  or  occasionally  with  the 
apex-beat,  and  for  its  interpretation  some  time  standards 


THE  VENOUS  PULSE  17 

and    a    pair    of    compasses    are    necessary.       The    time 
standards  are  the  following  : 

The  radial  pulse  follows  one-tenth  of  a  second,  and  the 
carotid  pulse  one-twentieth  of  a  second  after  the  onset  of 
ventricular  systole,  Avhich  in  its  turn  is  preceded  by  auric- 
ular  systole  by  one-fifth  of  a  second.  Before  the  tracings 
are  taken,  the  two  recording  pens  are  moved  up  and  down 
across  the  paper  to  mark  the  relative  positions  of  the 
venous  and  arterial  pulses  at  the  same  moment  of  time, 
and  to  give  the  "oi^dinate^^  for  accurate  measurement. 
A  time-recorder  constantly  marks  intervals  of  one-fifth 
(two-tenths)  of  a  second.  When  a  tracing  is  completed, 
the  distance  between  the  ordinate  for  the  artery  tracing 
and  the  beginning  of  the  upstroke  of  its  pulse-wave  is 
measured  accurately  with  the  compasses.  The  stretch 
between  the  points  of  the  compasses  is  then  decreased 
by  a  distance  exactly  equal  to  a  one-tenth  of  a  second 
interval  on  the  time- marker.  The  compasses  are  now 
applied  to  the  venous  pulse,  one  limb  being  placed  accu- 
rately on  its  ordinate,  and  the  other  on  the  tracing, 
where  it  will  fall  exactly  where  the  carotid  wave  ought 
to  be  developing.  This  spot  is  then  marked  as  the  rise 
of  the  c.  wave.  Each  successive  c.  wave  is  marked 
out  by  resetting  the  compasses  to  a  space  equal  to  the 
distance  between  the  commencement  of  the  upstroke  of 
the  arterial  pulse  tracings,  and  measuring  successive 
complete  pulse-waves  along  the  venous  tracing  from  the 
originally  marked  a.  wave,  marking  each  a.  wave  as 
before.  The  auricular  wave  ought  to  begin  two-tenths 
of  a  second  before  the  c.  wave. 

General  Inspection  in  Cases  of  Heart  Disease. 

The  general  inspection  should  always  be  carried  out 
with    the    patient  facing    a    good   natural   daylight,   as 

2 


18  HEART  DISEASE 

artificial  light  destroys  the  delicate  changes  in  shades 
of  colour,  especially  the  yellow  of  jaundice,  which  are 
such  important  indications  of  the  health.  Whilst 
patients  suffering  from  heart  disease,  even  in  its  most 
serious  forms,  may  look  "  the  picture  of  health,'^  with  a 
general  natural  freshness  of  complexion,  there  are  cer- 
tain signs  in  the  face  and  general  aspect  pointing  to 
cardiac  disease  which  are  visible  to  the  eye  of  a  skilled 
observer. 

The  g'eneral  sig'ns  are  those  of  shortness  of  breath 
on  slight  exertion,  or  even  without  any,  inability  to 
breathe  in  any  but  the  erect  position  (orthopnoea),  oedema, 
— especially  swelling  of  the  legs  and  dependent  parts. 
Marked  throbbing,  with  short  and  sudden  pulse-waves, 
in  the  carotid  or  other  arteries,  may  be  seen,  and  gener- 
ally means  aortic  regurgitation,  but  a  quickly  acting 
dilated  heart  may  cause  similar  appearances.  Distension 
of  the  veins  of  the  neck  with  or  without  visible  pulsation 
may  be  present. 

In  the  face,  in  addition  to  signs  of  the  general  dis- 
tress, there  may  be  seen,  but  not  always,  some  special 
changes. 

Mitral  stenosis  often  gives  rise  to  a  high  colour, 
localized  more  or  less  to  the  malar  eminences  of  the 
cheeks,  and  due  to  dilated  veins  (ven^  stellatas).  An 
exactly  similar  condition  is  met  with  in  people  who  have 
been  exposed  to  the  weather,  and  a  somewhat  similar 
condition,  and  one  which  often  deceives  the  student,  is 
met  with  in  myxoedema.  Here,  however,  there  is  a 
peculiar  yellowish,  waxy  appearance  of  the  rest  of  the 
face. 

In  aortic  disease,  when  it  is  severe,  there  is  generally 


INSPECTION  19 

much  pallor,  from  the  tendency  which  incompetence  of 
the  valve  has  to  empty  the  blood  vessels  rapidly,  and 
often  also  marked  '^  lines  "  running  from  the  nose  to  the 
outer  angle  of  the  mouth. 

Capillary  pulsation  may  be  seen  if  looked  for  care- 
fully over  the  forehead ;  but  to  see  this  properly  it  is 
generally  necessary  to  make  a  small  patch  of  blush  by 
rubbing  the  forehead  with  the  back  of  the  finger-nail. 

Cyanosis. — When  the  cardiac  muscle,  especially  that 
of  the  right  heart,  fails,  the  pulmonary  circulation 
cannot  be  carried  on  effectively,  with  the  result  that  the 
venous  blood  is  imperfectly  oxygenated.  It  then  collects 
in  the  systemic  circulation,  and  is  seen  in  the  skin  and 
mucous  membranes  as  a  bluish  discoloration,  or  cyanosis. 
Cyanosis  is  most  marked  in  dependent  parts,  the  lobes 
of  the  ears,  the  fingers  and  toes,  but  it  is  well  seen  in 
the  face.  This  form  of  cj^anosis  is  the  result  of  a  deficient 
force  pumping  blood  through  the  lungs. 

With  heart  disease  of  long  standing,  especially  of 
congenital  origin,  the  fingers  and  toes  are  often  clubbed 
as  well  as  purple. 

A  hluish,  ashy  grey  appearance  is,  however,  often  met 
with  in  chronic  bronchitis  and  emphysema  with  the  heart 
working  well.  This  is  due  to  inability  of  the  lungs  to 
expand  freely  and  oxygenate  the  blood  properly. 

In  congenital  heart  disease  there  is  generally  a  very 
deep  red,  purple,  or  bluish  aspect.  When  congenital 
heart  disease  is  met  with  in  people  over  puberty,  espe- 
cially over  twenty,  as  it  occasionally  is,  it  is  almost 
always  due  to  pulmonary  stenosis.  Other  congenital 
heart  lesions  generally  terminate  in  childhood,  but  I  saw 
one  adult  of  thirty-one  who  died  from  the  effects  of  a 


20  HEART  DISEASE 

congenital  septum  in  the  auricle,  which  simulated  mitral 
stenosis.    How  he  lived  as  long  as  he  did  was  a  wonder. 

Jaundice  is  also  often  present.  For  this  to  be  de- 
finitely established  the  conjunctivae  under  the  upper 
eyelids  must  be  examined^  the  yellow  discoloration  so 
often  seen  in  the  exposed  parts  not  being  due  to  bile 
pigments. 

Anxiety. — In  angina  pectoris  or  severe  intrathoracic 
aneurysm  there  is  often  an  appearance  of  extreme 
anxiety,  and,  if  the  pain  be  present,  of  great  distress. 

The  attitude  is  fixed  and  immobile  as  though  move- 
ment of  any  sort  were  feared,  in  marked  contrast  to  the 
excited  movements  of  hysterical  angina. 

Inspection  of  the  Neck. 

Arterial  pulsation. — Pulsation  or  throbbing  of  the 
carotid  arteries,  varying  in  degree,  will  often  be  seen,  a 
thin  neck  favouring  its  visibility.  In  the  majority  of 
cases  of  slighter  degree  it  means  nothing  abnormal,  merely 
a  favourable  position  of  the  arteries  for  their  pulsation  to 
reach  the  surface.  Even  when  marked  it  may  be  due 
simply  to  nervous  overaction  of  the  heart.  With  aortic 
regurgitation  it  reaches  its  highest  development,  when 
the  throbbing  of  a  soon-full,  soon-empty  vessel  is  very 
striking.  The  frontal  artery  may  also  be  seen  to  throb 
in  aortic  incompetence,  but  a  visible  pulse  wave  in  any 
exposed  artery  may  occur  without  any  heart  disease 
being  present.  In  dilatation  with  hypertrophy,  the 
carotid  arteries  may  pulsate  in  a  way  very  suggestive  of 
an  aortic  pulse. 

The  condition  of  the  veins  must  be  noted,  distension 
indicating  oljstruction  to  the  return  of  blood  to  the  right 


INSPECTION  21 

auricle,  or  to  its  flow  through  the  right  side  of  the  heart. 
The  jugular  veins  are  often  seen  to  be  very  full,  and  if 
examined  carefully  between  the  attachments  of  the 
sterno-mastoid  to  the  clavicle  and  sternum  pulsation  in 
them  may  be  seen  and  felt.  A  transmitted  impulse 
from  the  carotid  artery  must  be  discriminated  from  true 
venous  pulsation. 

The  direction  in  which  blood  flows  to  fill  the  veins  is 
important.  If  a  stretch  of  vein  be  emptied  between  two 
fingers  the  vein  will  fill  from  below  upwards  if  there 
is  tricuspid  regurgitation,  and  from  above  downwards 
when  auricular  distension  alone  or  venous  obstruction 
is  present. 

Any  general  swelling  of  the  neck,  if  present,  must  be 
noted,  as  it  is  generally  a  sign  of  serious  intra-thoracic 
disease  or  venous  obstruction. 

Inspection  of  the  Pr^cokdia. 

Inspection  of  the  preecordia  must  never  be  omitted,  as 
it  gives  most  valuable  information  in  disease.  A  side  or 
tangential  view  should  be  taken  if  the  direct  inspection 
is  negative,  pulsation  being  sometimes  seen  by  it,  and 
not  otherwise. 

The  normal  cardiac  impulse  may  be  invisible,  and 
negative  observation  may  mean  nothing  abnormal. 
The  anterior  and  mid-axillary  regions  should  be  most 
carefully  examined,  as  the  impulse  is  often  surprisingly 
far  out  in  disease. 

Diffuse  pulsation  between  the  mid-clavicular  line  and 
the  sternum  generally  means  disease  of  the  right  ven- 
tricle, and  widelj^  spread  pulsation,  outwards  as  well, 
means  enlargement  (dilatation  with  hypertrophy)  of 
both  ventricles.  Auricular  pulsation  is  never  seen. 
Pulsation  over  the  base  of  the  heart  generally  indicates 


22  HEART  DISEASE 

aneurysm  of  the  arch  of  the  aorta.  The  impulse  of  a 
forcibly  beating  normal  heart  may  extend  outwards  to 
the  nipple  line. 

Bulging  of  the  prcecordia  is  generally  best  seen  in 
children,  whose  chest  walls  give  easily  in  front  of 
enlarged  hearts.  When  limited  to  intercostal  spaces  it 
often  indicates  pericardial  eifusion. 

Systolic  retraction  of  the  interspaces  may  be  seen ;  it 
is  often  diffuse,  and  means  adherent  pericardium  or 
great  cardiac  enlargement,  the  contraction  of  the  heart 
causing  negative  pressure  in  the  thorax,  and  consequent 
retraction  of  the  intercostal  spaces. 

Palpation. 

Palpation  is  a  very  valuable  method  of  cardiac  diag- 
nosis, and  should  always  be  practised.  The  hand  must 
be  warm,  and  must  be  placed  over  the  region  of  the 
apex-beat  below  and  within  the  nipple  line.  As  much  of 
the  hand  as  possible  should  be  laid  over  the  praecordia, 
from  the  sternum  outwards,  with  the  region  of  the  distal 
interphalangeal  joints  about  where  the  impulse  is  ex- 
pected. As  the  prgecordia  are  often  very  tender,  a 
light  touch  must  always  be  used. 

Cardiac  Impulse. — When  the  impulse  is  felt  by  the 
hand,  the  outermost  limits  of  it  to  the  left  should  be 
determined  by  the  pad  of  one  finger  applied  in  the  inter- 
costal spaces.  This  gives  very  accurate  information  as 
to  the  area  of  heart  dalness,  which  will  be  further  in- 
vestigated later  by  percussion.  If  the  impulse  cannot 
be  felt  in  the  lying  position,  let  the  patient  sit  up  and 
lean  forward,  but  not  to  the  left ;  also  try  the  effect  of  a 
deep  expiration  and  the  holding  of  the  breath  after- 
wards. 


palpation'  23 

N.B. — The  heart  often  extends  surprisingly  far  into  the 
axilla,  and  mistakes  in  diagnosis  result  from  want  of 
attention  to  this  fact. 

An  absent  cardiac  impulse  may  mean  thick  chest 
walls^  with  too  much  adipose  tissue,  an  intervening  rib, 
emphysema,  feeble  heart  action,  or  pericardial  effusion. 

The  normal  apex-heat  has  characters  which  must  be 
learned  by  experience.  It  is  produced  by  systolic  con- 
traction and  elongation  of  the  heart,  the  elongation 
being  communicated  to  the  chest  wall  by  the  apex  of 
the  left  ventricle.  It  is  limited  in  area  to  that  of  about 
half,a  crown,  and  is  moderately  forcible  and  abrupt. 

In  disease  it  may  no  longer  be  an  apex-beat  from  the 
left  ventricle,  but  becomes  a  diffuse  impulse  from  the 
anterior  surface  of  the  right  ventricle. 

A  distinction  should  therefore  be  drawn  between  the 
apex=beat  and  the  cardiac  impulse. 

In  hypertrophy  of  the  heart  the  impulse  is  slow, 
heaving,  and  stronger  than  normal. 

In  dilatation  of  disease,  or  feeble  action  in  debility,  it 
is  quicker,  feebler,  and  more  slapping,  than  in  health. 

In  mitral  stenosis  the  accentuated  first  sound  can  be 
distinctly  felt,  and  should  be  a  definite  indication  of 
what  will  be  heard  on  auscultation  ;  a  thrill  may  be  felt. 

In  pulmonary  valve  lesions  an  accentuated  second 
sound  may  sometimes  be  felt  in  the  second  left  inter- 
costal space,  and  in  aneurysm  of  the  aorta  the  aortic 
second  sound  may  be  felt  as  a  diastolic  shock. 

Thrills  arising  within  the  heart  are  caused  by  pal- 
pable vibrations  set  up  in  the  diseased  valves  of  the 
heart  and  carried  to  the  surface  of  the  chest.  They 
arise  at  a  rigid  and  narrowed  orifice,  with  altered  curtains, 


24  HEART   DISEASE 

and  may  be  systolic  or  diastolic  in  rhythm.  The  sensa- 
tion of  liquid  being  sprayed  against  the  hand,  or  of  a 
cat  purring^  is  conveyed  l)y  them. 

Systolic  thrill  is  met  with  (a)  at  the  apex  of  the  heart 
in  regurgitation  through  a  mitral  or  tricuspid  valve 
made  incompetent  by  stenosis  ; 

(b)  At  the  base  in  obstruction  due  to  an  atheromatous 
aortic  valve.     A  pulmonary  thrill  is  extremely  rare.- 

Diastolic  thrill  is  met  with  (a)  at  the  apex,  with  blood 
entering  the  ventricle  through  a  stenosed  mitral  or 
tricuspid  valve. 

Regurgitation  through  an  incompetent  aortic  (or  pul- 
monary) valve  may  cause  a  thrill  over  the  ventricles. 

(h)  At  the  base  a  diastolic  thrill  is  extremely  rare. 

A  crescendo  thrill  is  felt  with  a  crescendo  murmur. 
The  rhythm  of  this,  as  usually  taught^  is  presystolic  or 
auricular  systolic — that  is^  just  before  the  systole  of  the 
ventricle.  As  will  be  seen  later,  the  rhythm  is  probably 
early  ventricular  systolic. 

Pericardial  friction  may  be  felt,  and  simulate  a  rough 
thrill,  but  it  has  not  the  character  of  sprayed  liquid, 
but  more  that  of  two  rough  surfaces  rubbing  together. 

Peecussion. 

Liyht  iwrcussion  gives  the  best  results,  and  should  be 
cultivated.  Changes  of  resonance  can  be  best  appre- 
ciated by  the  sensation  of  touch  aiding  that  of  sound. 
Apart  from  this,  the  pra^cordia  in  subjects  of  heart 
disease  are  often  exquisitely  tender,  and  most  patients, 
especially  in  private  practice,  prefer  gentle  methods. 
After  locating  the  outermost  limits  of  the  cardiac  im- 
pulse by  palpation,  the  heart  should  be  percussed  in  a 
routine  way,  and  always  from  resonance  to  dulness. 


PERCUSSION  25 

The  most  delicate  results  are  obtained  by  very  light 
percussion  in  an  intercostal  space,  thus  avoiding  the 
sounding-box  of  a  rib,  and  by  quick  contrasts  brought 
about  by  two  strokes  in  one  place  followed  quickly  by 
two  in  another  not  more  than  half  an  inch  away. 

Note  the  results  by  measurement  from  the  mid-sternal 
line,  the  normal  distance  in  an  adult  being  about  three 
and  a  half  inches  from  it. 

Routine  method  of  percussing*  out  the  heart 
dulness. — 

N.B. — It  is  very  important  to  follow  regularly  a 
definite  method  of  percussion  in  the  examination  of  the 
heart. 

1.  Limit  to  the  left. — Percuss  horizontally  along  the 
line  of  the  normal  apex-beat  from  the  axilla  inwards. 
If  the  heart  is  enlarged  or  displaced,  begin  to  percuss  a 
couple  of  inches  farther  out,  and  follow  along  its  changed 
horizontal  line. 

2.  Limit  to  the  right. — First  locate  the  liver  dulness 
(about  the  sixth  rib)  by  percussion  downward  in  right  mid- 
clavicular line.  Then  take  a  line  one  inch  above  this  and 
percuss  inwards  towards  the  sternum.  It  is  very  unusual 
to  get'  any  distinct  line  of  dulness  to  the  right  of  the 
sternum  in  health,  although  the  right  auricle  extends 
half  an  inch  in  this  direction,  the  ribs  and  sternum  acting 
as  a  sounding-box.  When  the  right  auricle  is  enlarged 
or  the  heart  displaced  to  the  right,  dulness  will  be 
found. 

3.  Limit  uijwards. — Percuss  in  a  line  one  inch  to  the 
left  of  the  sternum.  Dulness  will  be  found  about  the 
third  rib. 

4.  The  limit  downwards  is  the  upper  limit  of  the  liver 
and  diaphragm  against  which  the  heart  lies. 


26  HEART   DISEASE 

Superficial  or  absolute  cardiac  dulness  is  obtained 
over  the  small  triangular  part  of  the  heart  which  is  un- 
covered by  lung^namely,  that  bounded  by  the  mid- 
sternal  line,  a  line  running  from  it  at  the  level  of  the 
fourth  left  costal  cartilage  to  the  union  of  the  fifth  rib 
with  its  costal  cartilage,  with  its  base  line  at  the  level 
of  the  diaphragm  (sixth  rib). 

The  dulness  obtained  over  this  part  of  the  heart  with 
no  intervening  lung  is  more  marked  than  that  ob- 
tained over  the  deeper-seated  part  of  the  heart.  Its 
determination  is  not  important,  unless  it  is  to  note  the 
encroachment  of  an  emphysematous  lung  towards  the 
middle  line. 

Deep  cardiac  dulness  is  usually  that  sought  for  on 
percussion  of  a  heart.  Its  limit  is  that  of  the  heart  in 
the  chest.  The  more  lung  tissue  in  front  of  the  heart, 
the  less  absolute  is  the  dulness  obtained.  With  much 
emphysema  it  may  be  impossible  to  get  any  dulness 
at  all. 

Practical  points — in  health. — There  should  be  no 
dulness  to  the  right  of  the  sternum,  to  the  left  of  the  left 
mid-clavicular  line,  or  above  the  third  rib  on  a  line  one 
inch  to  the  left  of  the  sternum  in  the  adult. 

In  disease. — 1.  Dulness  to  the  right  of  the  sternum 
means  enlarged  right  auricle  or  displaced  heart.  Do 
not  forget  the  possibility  of  a  congenital  development  of 
the  heart  on  the  right  side. 

2.  Dulness  to  the  left  of  the  mid-clavicular  line  m^ans 
dilatation  of  the  left  ventricle  or  great  dilatation  of  the 
right  ventricle,  or  displacement  of  the  heart  to  the  left. 

3.  Dulness  below  the  fifth  costal  space,  in  the  region  of 
the  nipple  line,  means  hypertrophy  of  the  left  ventricle. 


AUSCULTATION  27 

In  hypertropliy  of  the  right  ventricle  pulsation  of  this 
ventricle  can  be  felt  under  the  costal  arch,  close  to  the 
xiphisternum. 

4.  Dulness  to  the  left  of  the  left  mid-clavicular  line 
and  helow  the  fifth  interspace  means  dilatation  and 
hypertrophy  of  the  left  ventricle  or  of  both  ventricles. 

5.  Dulness  above  the  third  rib,  due  to  cardiac  changes, 
means  pericardial  effusion.  The  whole  cardiac  dulness 
in  this  case  is  pear-shaped,  with  the  base  of  the  pear 
downwards,  and  the  cardiac  impulse,  when  it  is  felt,  is 
sometimes  well  within  the  outer  limits  of  dulness. 

Diminished  cardiac  dulness  means  emphysema  or 
pneumothorax. 

Extrinsic  causes  of  displacement  of  the  apex-beat. 

— The  whole  heart,  and  consequently  the  apex-beat,  may 
be  displaced  by  other  causes  than  those  which  arise 
within  the  heart  itself  or  within  the  pericardium. 

The  heart  may  be  pushed  out  of  place — 

(a)  By  intrathoracic  causes,  such  as  fluid  or  air  in  the 
pleural  cavities,  new  growths  or  aneurysm. 

(b)  Abdominal  causes,  ascites,  or  new  growths,  which 
push  up  the  diaphragm.  The  apex-beat  is  generally 
pushed  up  and  out  by  ascites. 

The  heart  may  be  pulled  out  of  place  by  shrinking  of 
the  lung,  especially  in  an  upward  direction,  as  by 
phthisis  of  the  upper  part  of  the  left  lung. 

Auscultation. 

A  wooden  stethoscope  gives  the  most  delicate  results 
in  auscultation,  but  a  binaural,  with  its  flexible  rubber 
tubes,  is  often  more  convenient.     The  use  of  both  may 


28  HEART   DISEASE 

be  cultivated  Avith  advantage.  Nothing  should  be 
allowed  to  rub  against  the  stethoscope,  otherwise  very 
alarming  auscultatory  phenomena  will  be  heard. 

N.B. — Theprsecordia  are  often  exquisitely  tender  in  heart 
disease,  and  the  stethoscope  chest-piece  must  be  applied 
with  this  in  mind. 

Localize  the  apex^beat.  Before  using  the  stethoscope^ 
it  is  of  the  utmost  importance  to  find  the  apex-beat  of 
the  heart,  or  the  outermost  limit  of  the  heart  to  the  left. 
Unless  this  be  done,  murmurs,  especially  the  crescendo 
murmur  heard  only  at  the  apex  of  the  left  ventricle  as 
a  rule,  may  be  overlooked. 

The  proper  way  to  use  a  stethoscope,  whether 
binaural  or  monaural,  and  with  the  patient  in  or  out  of 
bed,  is  to  place  one  hand  on  the  patient's  shoulder ^  and  to 
use  the  other  for  moving  the  stethoscope  from  place  to 
place.  This  not  only  prevents  the  examiner  from  adopt- 
ing the  unbusinesslike  and  objectionable  habit  of  keeping 
one  hand  in  his  pocket,  but  it  also  maintains  the  proper 
distance-relationship  between  the  examiner  and  the 
patient,  and  facilitates  the  timing  of  murmurs  by  the 
carotid  artery. 


Ill 

THE   HEART   SOUNDS 

It  is  important  to  bear  in  mind  the  anatomy  and 
mechanism  of  the  normal  valves  in  studying  the  changes 
ill  the  normal  heart  sounds  which  are  met  with  in 
disease. 

THE  FIRST  SOUND 

The  first  sound  is  produced  by  the  act  of  closure  of 
the  normal  mitral  and  tricuspid  valves  (auriculo- 
ventricular  or  a.-v.  valves)  by  the  contraction  of  the 
normal  ventricles. 

No  sound  is  heard  whilst  the  blood  is  passing  through 
the  a.-v.  valves  into  the  ventricles. 

Anatomy  of  the  auriculo-ventriculap  valves. — 

1.  The  fibrous^  inelastic  valve  curtains,  two  in  the  left, 
or  mitral,  valve ;  and  three  in  the  right,  or  tricuspid, 
valve.  From  the  edges  of  the  curtains  run  tendinous 
cords  (chordee  tendineae)  to — 

2.  The  musculi  papillares,  which  arise  from  the  muscle 
of  the  ventricular  wall. 

3.  Muscular  fibres  around  tlie  orifice  of  the  valves. 
It  used  to  be  taught  that  these  were  arranged  as  circular 
fibres,  but  recent  observations  suggest  that  in  addition 
to    some    circularly    disposed    fibres    the    spiral    muscle 

29 


30  HEART   DISEASE 

fibres  of  the  ventricle  are  attached  to  the  fibrous  valve 
ring  in  such  a  way  that  when  they  contract  they  help  to 
diminish  the  valve  orifice. 

Mechanism  of  the  closure  of  the  auriculo- ventri- 
cular valves. — 

1.  When  blood  is  passing  from  auricle  into  ventricle 
the  valve  curtains  lie  against  the  ventricle  wall  and 
offer  no  impediment  to  its  flow. 

2.  As  the  ventricle  fills  the  blood  floats  the  edge  of 
the  curtains  of  the  valves  into  such  a  position  that — 

3.  The  curtains  are  locked  in  competent  apposition  at 
the  very  onset  of  ventricular  systole  (v.s.),  when  the  papil- 
lary miiscles  are  said  to  contract^  and  before  the  intra- 
ventricular blood-pressure  has  reached  its  maximum. 

4.  At  an  early  phase  of  v.s.  the  "  circular  "  muscular 
fibres  contract,  and  so  reduce  the  areas  of  the  orifices  of 
the  valves .  that  the  curtains,  when  in  apposition,  com- 
petently close  the  valve  orifices. 

5.  The  force  with  which  the  ventricle  contracts  is 
determined  by  the  resistance  of  the  arterial  circulation, 
and  for  this  to  act  with  maximum  efficiency  the  valves 
must  be  competent.  The  greater  the  resistance  to  its 
contraction,  the  more  vigorous  is  the  systole  of  the 
ventricle,  within  certain  limits. 

Causation  of  the  normal  first  sound. — The  first  sound 
of  the  heart  is  caused  by — 

1.  Vibration,  or  tension,  set  up  in  the  curtains  of  the 
mitral  and  tricuspid  (a.-v.)  valves  by  the  force  of  intra- 
ventricular blood-pressure  which  closes  the  valves.  This 
is  the  dominant  factor  in  the  causation  of  the  first  sound. 

2.  Muscle  vibration,  or  tension,  in  the  contracting  walls 
of  the  ventricles. 


FIRST  SOUND  31 

3.  Arterial  tension.  There  must  be  a  certain  amount 
of  pressure  in  the  arteries  to  afford  that  resistance 
which  is  necessary  for  the  ventricles  to  contract  with 
a  certain  degree  of  deliberation  and  force. 

There  is  a  considerable  degree  of  elcisticity  in  forces 
2  and  3. 

The  valve  curtain  note  is  of  higher  pitch  than  the 
muscle  note,  but  the  sound  cannot  be  resolved  into  its 
component  parts  by  the  ear. 

iSTo  sound  is  heard  whilst  blood  passes  through  the 
normal  open  valves  into  the  ventricles. 

The  Mitral  sound  louder  than  the  Tricuspid  sound, 

— The  left  side  of  the  heart,  though  more  deeply  seated, 
is  the  predominant  partner  in  the  causation  of  the 
first  sound,  because  the  blood-pressure  which  acts  in 
closing  and  maintaining  competent  its  valves  is  two  or 
three  times  greater  in  the  left  ventricle  and  the  aorta 
than  in  the  right  ventricle  and  pulmonary  artery.  This 
suggests  that  the  valves  of  the  left  side  of  the  heart 
close  with  twice  or  thrice  the  tension  of  the  valves  of 
the  right  side. 

Location  of  the  apex-beat. — The  importance  of 
localizing  the  apex  of  the  heart  as  accurately  as 
possible  by  palpation  or  percussion,  or  b}^  both 
these  methods  of  examination,  has  been  referred  to 
under  the  section  on  Auscultation.  This  point 
cannot  be  emphasized  too  much,  for,  unless  the 
stethoscope  be  placed  over  the  left  ventricle,  sounds  or 
murniurs  produced  at  the  mitral  valve  may  he  entirely 
overlooked. 

When  the  heart  is  enlarged  and  the  right  ven- 
tricle is  dilated,  the  true  apex  of  the  heart  (the 
apex  of   the  left  ventricle)    may   not  come   to   the 


82  HEART  DISEASE 

surface,  but  by  finding  the  outermost  limit  of  the 
heart  to  the  left  we  get  as  near  to  it  as  possible, 
and  reduce  possible  errors  to  a  minimum. 

Characteristics  of  the  first  sound. — The  normal  first 
sound  is  dull  and  deliberate,  and  is  imitated  by  the 
sound  nhbj  as  compared  with  the  higher  pitched, 
shorter  sound  produced  at  the  semilunar  valves,  imitated 
by  the  sound  vjj.  To  produce  this  sound,  tension  in  the 
curtains  of  the  closed  a.-v.  valves  and  in  the  contracting 
muscle  of  both  ventricles,  and  the  blood-pressure  in 
the  arteries  must  be  normal 

There  is  some  degree  of  elasticity  in  the  papillary 
muscles  acting  on  the  a.- v.  valves,  like  sailors  holding 
the  ropes  of  a  flapping  sail,  which  probably  prevents 
sudden,  inelastic  tension  of  the  curtains,  and  produces 
a  note  of  lower  pitch  than  that  developed  at  the  rigid 
inelastic  curtains  of  the  semilunar  valves,  which  may,  to 
continue  the  simile,  be  compared  with  a  flapping  sail 
fixed  to  the  rigid  sides  of  the  ship. 

To  summarize,  then,  the  first  sound  is  produced  by 
tension  of  the  a.-v.  valve  curtains  and  of  the  ventricle 
muscle  of  the  right  and  left  sides  of  the  heart,  and  is  a 
double  compound  sound,  though  it  is  caused  chiefly  by 
the  mitral  valve  and  left  ventricle. 

Time. — It  is  important  to  note  that  the  first  sound  is 
developed  at  an  early  phase  of  v.s.,  and  only  occupies 
the  first  part  of  this  event. 

A  first  sound  can  therefore  he  continued,  ov  followed,  by 
a  murmur  produced  at  a  later  phase  of  v.s.  (in  a  manner 
to  be  described  later)  through  defects  at  the  same  valve 
orifice  tchlch  allow  of  ^regurgitation  of  blood  into  the 
auricle  during  the  coniph'tion  of  v.s.  (systolic  murmur). 


FIRST  SOUND  33 

Distinctness. — The  distinctnes.s  witli  wliich  tXm  normal 
fimt  sound  of  the  heart  can  be  heard  over  the  pra^cordia 
depends  on — 

(1)  The  thickness  of  the  structures  ivhich  intervene 
between  the  heart  and  the  stethoscope.  Thus^  much 
adipose  tissue  in  the  chest  wall  will  diminish  the  sound, 
as  also  will  an  emphysematous  lung  pushing  forwards 
over  the  heart,  or  pericardial  fluid  displacing  the  apex. 

(2)  The  force  of  the  contractimj  ventricle.  A  forcibly 
contracting  ventricle,  as  in  nervous  palpitation,  or  after 
exertion,  makes  the  sounds  so  loud  that  they  can  be 
heard  by  the  subject  himself,  or  by  an  observer  at  a 
short  distance  from  tlie  chest,  without  the  help  of  any 
conducting  medium. 

On  the  other  hand,  a  feebly  heating  normal  heart,  as 
in  debility,  or  syncope,  or  '^  fainting,"  gives  rise  to  a 
correspondingly  feeble  first  sound. 

Modifications  of  the  Fiest  Sound. 

Departures  from  the  normal  condition  of  the  valve 
curtains,  cardiac  muscle  and  blood-pressure  which  pro- 
duce the  normal  first  sound,  will  modify  the  character 
of  the  sound,  or  produce  additional  audible  signs. 

I. — Chang-es  in  the  valve  curtains  may  modify  the 
sound. — 

1.  Weakening  or  absence  of  the  sound. — The  curtains  of 
the  valve  may  be  more  or  less  stiffened  by  disease  so  that 
they  can  only  close  slowly  or  that  they  cannot  close  at 
all.  The  sound  will  then  be  modified,  or  it  will  not  be 
heard  at  all. 

2.  Production  of  Tnurmtirs. — When  the  curtains  are  so 
diseased  that  they  are  unable   to   move  and  close  the 

3 


34  HEART   DISEASE 

valve,  they  not  only  no  longer  produce  a  sound,  but  they 
may  cause  the  development  of  a  murmur  of  incompe- 
tence.    This  new  sign  will  be  referred  to  fully  later. 

3.  Accentuated  sounds. — When  thickened  by  disease, 
but  still  able  to  close  more  or  less  competently,  the 
curtains  may  come  together  with  a  snap  or  markedly 
accentuated  sound.  Such  an  unusually  sharp  and 
accentuated  first  sound  is  best  heard  in  a. v.  stenosis. 

4.  Perforation  of  the  curtains  through  ulceration  may 
lead  to  the  production  of  a  murmur  with  or  without 
a  first  sound,  according  to  whether  the  valve  is  or  is 
not  too  much  diseased  to  produce  a  sound. 

II. — Changes  in  the  muscle  of  the  ventricle  may 

modify  the  first  sound  in  two  ways  : 

1.  Thickening,  or  ti'tie  hypertrophy,  with  slower,  more 
deliberate  and  more  forcible  contraction  of  the  heart 
muscle,  and  a  less  sudden  development  of  tension  in  the 
curtains,  as  compared  with  normal,  gives  rise  to  a  note 
which  is  of  lower  pitch,  more  lengthy  duration,  and  is 
dull  or  muffled,  as  compared  with  the  normal  first  sound. 

The  thickened  ventricular  wall  probably  aids  further 
in  the  production  of  this  dull  sound  by  hindering  con- 
duction of  the  valve  tension  element  of  the  sound. 

2.  Thinning  of  the  wall,  as  in  dilatation  of  the  ven- 
tricle, on  the  other  hand,  owing  to  the  quicker  and  less 
efficient  contraction  of  the  heart  muscle  and  more  in- 
elastic production  of  curtain  tension,  causes  a  note  which 
is  more  abrupt  and  slapping  and  of  higher  pitch  than 
the  normal  sound.  The  unusually  thin  walls  of  the 
ventricles  probably  facilitate  the  hearing  of  the  valve 
tension  element  of  the  sound. 

In  marked  cases  of  dilatation  of  the  ventricles  the 
sound  heard  is  probably  mostly  one  of  valvular  tension. 


FIRST   SOUND  35 

the  papillary  muscles  contributing  to  tliis  effect  ])y  losing 
their  elastic  pull  on  the  valve  curtains. 

3.  Any  structural  changes  in  the  walls  of  the  ventricle 
which  (a)  diminish  the  force  of  contraction ,  such  as  myo- 
carditis, fatty  degeneration  or  infiltration,  will  diminish 
the  loudness  of  the  first  sound ;  or 

{}))  Any  changes  which  diminish  its  ela,sticity,  such  as 
fibroid  degeneration^  will  accentuate  the  sound. 

III. — Changes  in  blood-pressure  also  have  an  effect 
on  the  heart  sounds.  A  high  pressure,  generally  asso- 
ciated with  some  muscle  hypertrophy  or  increased  force 
of  heart-beat  causes  a  more  vigorous  ventricular  con- 
traction and  a  louder  sound  than  a  low  blood-pressure, 
Avhich  tends  to  weaken  the  sounds. 

IV. — An  association  of  two  or  more  of  the  above- 
mentioned  factors  which  modify  the  first  sound  of  the 
heart,  a  condition  frequently  met  with  in  heart  disease, 
will  cause  more  marked  changes  in  it. 

A  weak  or  absent  first  sound  will  result  from — 

1.  Changes  in  the  valve  curtains  which  interfere  with, 
or  do  away  with  altogether,  the  development  of  tension 
in  them  at  the  onset  of  v.s.  The  valve  curtains  may 
become  so  thick  and  stiff,  forming  a  permanent  funnel- 
shaped  passage,  that  they  are  immovable,  and  cannot  be 
closed  or  thrown  into  tension.  No  valve  sound  is  then 
heard,  a  murmur  of  regurgitation  or  incom'petence  taking 
its  place ;  a  murmur  of  obstruction  is  also  generally 
heard  during  the  passage  of  blood  in  the  proper  direction 
through  the  valve. 

2.  Feehle  action  of  the  heart,  as  in  debilitated  states, 
after  continued  fever,  or  during  faintness. 


36  HEART    DISEASE 

3.  Pericardial  effusion,  when  there  is  a  fair  amount 
of  fluid  present. 

4.  Diminution  of  the  hlood-pressure. 

Accentuation  of  the  first  sound. — The  term  ac-cen- 
tuation  is  generally  applied  to  the  first  sound  heard  in 
abnormal  conditions,  in  which,  however,  the  valve  curtains 
are  either  normal,  or  not  diseased  enough  to  aifect  their 
mobility. 

1.  The  tone  is  clearer,  sharper,  shorter  than  normal. 
Such  an  accentuated  sound  is  heard  with  dilated  ven- 
tricles, in  which  there  is  a  more  sudden  stretching  of 
the  valve  curtains  owing  to  the  weak,  inelastic  condition 
of  the  papillary  muscles.  It  is  also  heard  when  the 
hlood-jyressiire  is  increased. 

2.  The  dull,  prolonged,  and  thudding  note  of  ven- 
tncular  hypertropliy  is  much  muffled  in  its  conduction  to 
the  surface  by  the  thickened  ventricular  wall. 

3.  When  the  thickened,  almost  cartilaginous  valves 
of  a.'V.  stenosis  come  together,  they  produce  an  abrupt 
and  accentuated  sound  which  is  characteristic  of  this 
form  of  valvular  disease. 

4.  When  a  heart  is  lying  in  contact  with  a  stomach 
distended  with  air  or  gas,  the  sounds  may  have  a  peculiar 
"  tympanitic  "  ring,  which  disappears  when  the  flatulent 
distension  passes  off. 

Reduplication  of  the  first  sound.  —  Normally  the 
ventricles  contract  synchronously,  and  give  rise  syn- 
chronously to  the  sounds  which  blend  into  what  we 
hear  as  the  single  first  sound.  We  often  hear,  however, 
the  single  first  sound  replaced  by  two  sounds — that  is, 
by  reduplication  or  doubling.  An  excellent  imitation  of 
the  single  or  double  first  sound  can  be  made  by  striking 
on  the  forehead  by  two  fingers  synchronously,  and  then 


FIRST   SOUND  37 

with  varying   interval  between  the  contact  of  the  two 
fingers  with  the  forehead. 

The  distinctness  of  the  double  first  sound  may  vary 
from  a  slight  degree  which  has  been  imitated  by  the 
sound  truj)  to  one  in  which  the  two  component  sounds 
are  quite  separate  (ter-up).  These  variations  can  be  well 
imitated  Avith  the  fingers  on  the  forehead. 

The  explanation  of  a  double  first  sound  which  is 
usually  given  is  want  of  synchronism  of  ventricular 
contraction  generally  due  to  abnormalities  of  blood- 
pressure  in  the  two  circulations.  If  one  ventricle  has 
more  work  to  do  than  in  the  normal  condition  of  affairs, 
it  is  said  that  it  will  reach  that  part  of  its  systolic  phase 
at  which  the  first  sound  is  produced  earlier  than  does 
the  other  ventricle,  and  so  produce  the  double  first  sound. 

This  explanation  of  reduplication  of  the  first 
sound  of  the  heart  is  not  without  objection.  To 
begin  with,  the  blood-pressure  in  the  left  ventricle 
and  the  aortic  circulation  is  two  or  three  times  as 
great  as  that  in  the  right  ventricle  and  pulmonary 
circulation ;  but,  on  the  other  hand,  the  wall  of  the 
left  ventricle  is  correspondingly  thicker,  and  there- 
fore more  powerful  than  that  of  the  right  ventricle. 
If  the  blood-pressure  in  one  of  the  circulations  is 
increased,  one  of  two  things  results  : 

1.  More  muscle  is  developed  —  compensatory 
hypertrophy — to  deal  with  this  increased  pressure, 
and  therefore  this  ventricle  is  enabled  to  start  on 
level  terms  with  the  contraction  of  the  other  ven- 
tricle ;  or — 

2.  Dilatation  of  the  ventricle  and  muscle  in- 
capacity results,  with  dilatation  of  the  valve  and 
consequent  regurgitation.     This  safety-valve  action 


38  HEART  DISEASE 

relieves  the  increased  pressure  on  the  overworked 
muscle,  and  again  takes  away  any  handicap  as 
between  the  ventricles. 

Physiology  teaches  us  that  normally  the  left  side 
of  the  heart  commences  its  contraction  about  one- 
fiftieth  of  a  second  before  the  right,  but  this 
difference  is  imperceptible  to  the  human  ear. 

It  seems  to  me  that  we  may  have  another  explana- 
tion of  the  double  first  sound  when  it  occurs  with 
actual  or  relative  weakness  of  the  papillary  muscles 
of  one  or  both  ventricles.  The  intraventricular 
blood-pressure  is  at  its  highest  after  the  contraction 
of  the  papillary  muscles,  which  occurs  at  the  earliest 
phase  of  v.s. ;  but  whilst  the  papillary  muscles 
maintain  their  systolic  contraction  as  long  as  that 
of  the  ventricle  persists,  in  the  normal  condition  of 
affairs,  it  seems  quite  possible  in  disease  of  the 
ventricle  muscle,  or  in  abnormal  pressure  in  the 
ventricles — such  as  is  met  Avith  in  an  increased 
arterial  tension — for  the  papillary  muscles  to  fail 
after  their  initial  contraction,  but  before  the  systole 
of  the  ventricle  is  completed,  and  allow  the  valves 
to  fly  back  and  to  be  put  suddenly  into  a  state  of 
secondary  tension  by  the  stretching  of  the  musculi 
papillares  and  the  chordas  tendineas.  At  any  rate, 
it  is  in  conditions  which  cause  increased  arterial 
pressure,  and  in  muscle  failure  of  the  ventricle  with 
or  without  abnormal  blood-tension  that  we  get  the 
double  first  sound. 

Clinical  sigriificance  of  double  first  sounds. — 
1.  Functional   causefi. — Doubling    of    the    first   sound 
may  not  have  any  pathological  significance — that  is,  it 
may  be  heard  with  no  organic  lesion.     It  may  occur  at 


SECOND  SOUND  39 

the  end  of  full  expiration  and  the  beginning  of  inspira- 
tion on  deep  breathing. 

2.  07'ganic  causes. — A  double  first  sound  may  be  a 
physical  sign  of  severe  disease  in  which  increased  arterial 
tension  develops,  or  in  which  the  heart  muscle  fails. 
In  this  latter  case  the  rhythm  of  the  cardiac  cycle  is 
altered,  and  the  first  sound  follows  the  second  abnormally 
quickly  (see  Rhythm  of  Sounds  of  the  Heart  and  Bruit 
de  Galop,  p.  45). 

Doubling  of  the  first  sound  is  not  a  special  sign  of  any 
form  of  valvular  disease. 

THE  SECOND  SOUND 

The  second  sound  is  produced  by  the  act  of  closure  of 
the  normal  aortic  and  pulmonary  valves  by  the  intra- 
arterial blood-pressure. 

No  sound  is  heard  whilst  blood  passes  through  the 
normal  open  semilunar  valves  into  the  aorta  or  j)uliTion- 
ary  artery. 

Anatomy  of  the  semilunar  valves. — The  semilunar 
valves  at  the  aortic  and  pulmonary  orifices  consist  of 
fibrous,  inelastic  valve  curtains,  three  in  each  valve. 
These  curtains  are  attached  by  their  bases  to  the  fibrous 
ring  of  the  valve  orifices,  which  also  contains  a  little 
elastic  tissue. 

There  is  nothing  in  the  semilunar  valves  to  compare 
with  the  musculi  papillares  or  the  chordae  tendineae  of 
the  a.-v.  valves. 

Mechanism  of  the  closure  of  the  semilunar  valves. — 

1.  Whilst    blood  is  being  driven  into  the  aorta   and 

pulmonary  artery  the  curtains  of  the  semilunar  valves 

are  closely  apposed  to  the  wall  of  the  vessels  so  as  to 


40  HEART  DliSEASE 

offer  no  resistance  to    the    flow  of    blood   through   the 
valve. 

2.  The  curtains  of  the  valves  are  locked  in  competent 
apposition  when  the  pressure  in  the  large  arteries  is 
greater  than  the  driving  force  of  the  ventricles. 

Causation  of  the  normal  second  sound.— The  second 
heart  sound  is  caused  only  by  tension^  and  has  no  muscle 
element  in  it. 

No  sound  is  heard  whilst  blood  passes  through  the 
normal  open  valves  into  the  large  arteries. 

The  rlosure  of  the  semilunar  valves  is  brought  about  by 
an  elastic  force — namely,  the  contraction  of  the  muscle 
fibres  and  the  elastic  tissue  of  the  walls  of  the  aorta  and 
pulmonary  artery.  It  is  important  to  remember  this, 
because  loss  of  elasticity  in  the  wall  of  the  large  arteries 
through  vascular  sclerosis  modifies  the  sound. 

N.B. — This  force,  which  may  be  called  the  systolic 
contraction  of  the  aorta  or  pulmonary  artery,  is  at  its 
maximum  in  its  earliest  phase,  and  not  at  a  later 'period, 
as  in  the  case  of  ventricular  contraction. 

This  elastic  force  gives  rise  to  one  act  of  curtain 
tension  and  one  sound  in  each  of  the  two  valves. 
This  action  may  be  compared  to  the  single  sound 
which  can  be  made  when  an  inelastic  object — e.g., 
a  hammer  (the  column  of  blood  in  the  arteries) — is 
brought  suddenly  against  an  inelastic  resistance — 
e.g.,  an  anvil  (the  valve  curtains) — by  an  elastic 
force — e.g.,  the  muscles  of  the  arm  governed  by  the 
will  (the  elastic  structures  in  the  arterial  wall). 
On  the  other  hand,  if  the  inelastic  hammer  is 
allowed  to  fall  by  its  own  weight  on  the  inelastic 
anvil,  a  double  sound  of  primary  and  rebound 
impact  will  result.     The  importance   of   this  point 


SECOND  SOUND  41 

will    be  seen  when   we    speak  of  reduplication   or 
doubling"  of  the  second  sounds. 

The  normal  second  sound^  then^  is  a  compound  .sound, 
being  caused  by  the  closure  of  the  aortic  and  pulmonary 
valves ;  but  as  the  blood-pressure  in  the  aorta  is  two  or 
three  times  as  great  as  that  in  the  pulmonary  artery, 
the  aortic  valve  probably  contributes  chiefly  to  its 
causation.  On  the  other  hand,  the  deeper  situation  of 
the  aortic  valve  must  be  borne  in  mind. 

Any  second  sound  heard  over  the  carotid  arteries  is 
aortic  in  origin. 

Characteristics  of  the  second  sound. — Normally  the 
second  sound  has  definite  characteristics  of  pitch  and 
duration.  It  is  sharper  and  shorter  than  the  first  sound, 
being  imitated  by  the  sound  tip,  as  compared  with  ubb 
of  the  first  sound,  and  suggests  valve  tension  only  as  its 
causative  agent. 

Time. — The  second  sound  is  developed  at  the  very 
outset  of  v.d.,  and  therefore  it  can  be  followed  by  any 
abnormal  sound  which  may  be  produced  at  a  defective 
valve  during  the  remainder  of  v.d.  (diastolic  murmur). 

Distinctness. — The  conditions  which  affect  the  audi- 
bility of  the  normal  first  sound — namely,  thickness  of 
intervening  structure,  force  of  heart-beat — will  also 
affect  that  of  the  normal  second  sound. 

Modifications  of  the  Second  Sound. 

Modifications  of  the  condition  of  the  semilunar  valve 
curtains,  of  the  elasticity  of  the  arterial  wall,  and  of  the 
blood-pressure,  will  modify  the  second  sound,  much  as 
similar  changes  modify  the  first  sound. 


42  HEART   DISEASE 

I. — Changes  in  the  valve  Curtains  may  modify  the 
sound. — 

1.  Weakening  or  absence  of  the  sound. — The  curtains 
of  the  valve  may  be  so  stiffened  by  disease  that  they 
cannot  close  at  all  or  can  only  close  slowly.  The  sound 
will  then  not  be  produced  at  all,  or  it  will  be  modified. 

2.  Production  of  Murmurs. — When  the  curtains  are  so 
diseased  that  they  are  unable  to  move  and  close  the 
^alve,  they  not  only  no  longer  produce  a  sound  but  they 
may  cause  the  development  of  a  murmur.  This  new 
sign  will  be  referred  to  fully  later. 

3.  Accentuated  sounds. — With  the  curtains  diseased, 
but  still  able  to  close  competently,  the  sound  of  closure 
is  more  accentuated,  and  may  be  followed  by  a  murmur. 

4.  Perforation  or  injury  to  a  curtain  may  occur  in 
aortic  disease  after  unusually  severe  and  sudden  exer- 
tion. Some  sound  of  tension,  followed  by  a  murmur 
of  incompetence,  is  then  heard. 

II. — Changes  in  the  wall  of  the  artery. — 

1.  Loss  of  elasticity  from  atheromatous  degeneration 
of  the  middle  coats  leads  to  a  more  abrupt  a(;centuated 
sound  of  tension. 

2.  When  the  above  change  is  followed  by  dilatation 
of  the  artery  (especially  of  the  aorta),  the  second  sound 
is  often  of  a  peculiar  ringing  character,  which  may  be 
the  first  sign  of  the  condition  of  the  aorta. 

III. — Changes  in  the  blood-pressure  affect  the  second 
sound  very  markedly,  accentuating  it  when  it  is  ab- 
normally high  (increased  tension),  and  diminishing  it 
when  it  is  abnormally  low. 

A  feeble  or  weak  second  sound  will  be  heard  when 


SECOND  SOUND  43 

the    arterial   blood -pressure    is    abnormally  low,  and  is 
generally  associated  with  a  weak  first  sound. 

The  second  sound  may  be  ahseyit  altogether  if  the 
valve  curtains  are  so  stiffened  by  disease  as  to  be  unable 
to  come  together  during  v.d.,  or  to  be  thrown  into  a  state 
of  tension  sufficient  to  produce  a  sound. 

Accentuation  of  the  second  sound. — Physiologically, 
this  occurs  at  the  end  of  deep  inspiration  and  the  begin- 
ning of  the  following  expiration,  and  can  be  brought  on 
by  holding  the  breath. 

In  disease  it  is  very  common  to  hear  the  aortic  second 
sound  accentuated  when  arterial  tension  is  high,  especi- 
ally in  Bright^s  disease,  and  the  pulmonary  second  sound 
in  congestion  of  the  leseer  circulation,  especially  in  mitral 
regurgitation. 

Accentuation  of  the  second  sound  is  often  associated 
with  accentuation  of  the  first  sound  in  these  conditions. 
.  Ringing  Sound. — In  one  condition  in  which  there  is  an 
abnormally  large  amount  of  blood  just  above  the  valve — 
aneurysm  of  the  aorta — the  second  sound  has  a  peculiar 
accentuated  ringing  sound,  which  may  be  the  only  aus- 
cultatory sign  of  aneurysm  of  the  first  part  of  the 
aorta. 

Effect  of  Thickened  Curtains  on  the  Sound. — ^^[ormally 
the  edges  of  the  cusps  of  the  valves  which  come  into 
contact  on  closure  of  the  valve  are  very  fine  and  uni- 
formly smooth,  and  no  sound  of  impact  is  caused  from 
the  way  in  which  they  are  ^'  floated "  into  apposition 
before  the  final  locking  in  competent  closure.  If  the 
edges  of  the  cusps  of  the  valve  be  thickened  or  calcareous 
whilst  the  cusps  are  still  capable  of  coming  into  compe- 
tent apposition,  an  accentuated  sound  may  be  produced 
by  the  impact  of  these  cusps. 


44  HEART   DISEASE 

Reduplication  of  the  second  sound. — A  double  second 
sound  is  usually  said  to  mean  asynchronous  closure  of  the 
aortic  and  pulmonary  valves,  and  to  be  due  to  a  higher 
blood-pressure  in  one  of  the  circulations  which  induces 
abnormally  early  closure  of  the  valve  of  the  artery  in 
question. 

[A  fallacy  in  this  teaching  suggests  itself  at  once 
—  namely,  that  as  the  pressure  in  the  aorta  is 
normally  twice  or  thrice  that  in  the  pulmonary 
arter}^,  we  should  get  reduplication  of  the  second 
sound  normally. 

It  is  not  the  amount  of  pressure  in  the  large 
arteries,  then,  that  determines  the  time  of  closure 
of  the  semilunar  valves.  They  close  when  the 
pressure  in  the  arteries  is  greater  than  that  in  their 
corresponding  ventricles ;  so  if  asynchronism  of 
closure  of  the  semilunar  valves  is  to  occur,  it  must 
be  because  one  ventricle  takes  longer  to  drive  blood 
into  its  artery  than  the  other,  not  because  there  is 
abnormal  pressure  in  the  aorta  or  pulmonary  artery. 
Thus,  a  dilated  ventricle  may  be  pumping  blood 
into  its  artery  for  a  longer  time  than  the  other 
ventricle,  or  a  badly  filled  ventricle  (often  met  with 
in  mitral  stenosis)  may  pump  its  blood  into  the  aorta 
sooner  than  the  normal  or  dilated  right  ventricle. 
In  both  these  cases  double  second  sounds  would  be 
heard. 

It  is,  however,  quite  possible  for  an  increase  in 
the  blood-pressure  of  the  aorta  or  pulmonary  artery 
to  give  rise  to  a  double  second  sound  by  causing  a 
rebound  of  tlie  column  of  blood  which  throws  the 
semilunar  valves  into  sound-producing  tension,  such 
a  rebound  being  due  to  a  want  of  elasticity  in  the 


TIC-TAC  RHYTHM  45 

vessel  wall  which  frequently  accompanies  increased 
tension.  In  this  case  there  would  be  a  comparatively 
inelastic  force  closing  the  valve,  and  with  this  re- 
bound a  double  sound  would  result  in  the  manner 
described  on  a  previous  page  (p.  46).] 

The  rhythm  of  the  first  and  second  sounds  is  of 
very  great  importance  in  the  diagnosis  of  the  condition 
of  the  heart  muscle,  and  may  be  referred  to  here. 

In  a  normal  heart  beating  seventy- five  times  per  minute 
the  whole  duration  of  a  cardiac  cycle  is  0*8  second.  Of 
this  time  OS  is  occupied  by  v.s.  and  0-5  by  v.d.    As  the 


M 


1 — \ — iA»  r  I    I    r   ^    r 

V5       ■  VD  ' 

Fig.  4. — Khythm  of  Noiimal  Sounds  of  a  Heaiit  beating 
75  PER  Minute. 

YS   equals  three-tenths  ;    VD,  iive-tenths  ;   auricular  systole,  one-tenth 
second.     All  the  figures  are  thus  spaced  except  Figs.  5  and  6. 

first  and  second  sounds  occur  at  the  beginning  and  end 
respectively  of  v.s.,  it  follows  that  there  is  a  longer 
interval  between  the  second  and  first  than  between  the 
first  and  second  sounds  in  the  proportion  of  5  to  3.  This 
relative  duration  of  the  intervals  between  the  heart 
sounds  is  maintained,  and  can  be  recognized  in  hearts 


1 — r — I — J" — 1 — [■ — I — r    I     r — ] — \ — I — I — I — I — r 

VS      VD      V5     VD 

Fig.  5.— Tic-Tag  RhytHxM. 

Space  between  first  and  second  and  second  and  first  sounds  equal. 
Diastolic  rest  much  shortened. 

beating    rapidly — 120    to    130  per  minute.     When   the 


46  HEART  DISEASE 

time  intervals  between  the  sounds  become  equal — tlie 
so-called  "tic-tac"  or  "embryocardial"  rhythm;  or  when 
the  second  sound  follows  too  quickly  on  the  first  sound, 
and  there  is  a  proportionately  longer  pause  between  the 
second  sound  and  the  following  first  sound,  it  is  most 
probable  that  there  is  some  lesion  of  the  cardiac  muscle 
(see  later,  p.  47). 


u 


"1 — J — I — I — I — J — » — J — I — I — I — J — I — J — ? — I — r 

VS.  VD. 

Fig.  6. 

Space  between  second -and -first  sounds  too  short.     Diastole 
comparatively  prolonged. 

Cantering'  rhythm,  or  Bruit  de  galop. — In  its  slighter 
degrees,  reduplication  of  the  first  or  second  sounds  of 
the  heart  is  not  readily  recognized  by  the  beginner,  but 
familiarity  with  the  peculiar  characteristics  of  the  ab- 
normal sound  can  be  obtained  by  practising,  as  de- 
scribed previously  (p.  36),  its  imitation  by  the  finger  tips 
on  the  forehead.  The  more  marked  degrees  of  redupli- 
cation are  easily  recognized,  and  the  only  difficulty  is  to 


P 


T—] — ! — I — I — r—] — I — I    T   ^    I — I — I — » — I — 

V5.  V.O.  VS.  VD. 

Fig.  7.— Bruit  de  Galop. 

Double  first  and  single  second  sound,  and  single  first  and  double 

second. 

determine  which  of  the  sounds  is  doubled — a  difficulty 
which  is  removed  by  timing  them  by  the  carotid  artery. 
The  carotid  pulse  follows  the  onset  of  ventricular  systole 
at  an  inappreciable  interval  of  only  0*05  second.    There- 


BRUIT  DE  GALOP  47 

fore  any  sounds  which  are  synchronous  with  the  carotid 
pulse  are  synchronous  with  ventricular  systole,  and  any 
which  are  not  are  synchronous  with  ventricular  diastole 
(see  Timing  of  Murmurs). 

When  reduplication  is  marked,  and  one  of  the  three 
sounds  is  accentuated,  the  rhythm  suggests  the  simile  of 
a  cantering  or  galloping  horse  ;  hence  the  name  which 
is  often  applied  to  the  condition.  It  may  be  phonetically 
represented  by  the  sounds  luh  terup,  luh  ferup,  or  terup 
tup,  temp  tup.  Any  one  of  the  three  sounds  may  be  the 
most  accentuated. 

Whatever  pathological  significance  reduplication  of 
the  first  or  second  sounds  of  the  heart  may  have  when 
the  sounds  maintain  their  relative  distance  from  each 
other,  the  prognosis  is  much  icorse  ivhen  the  first 
sound,  whether  single  or  double, /b//oi«.9  mo7-e  closely  on 
the  second,  whether  single  or  double,  thari  it  ought  to. 
This  means  that  the  ventricles  are  not  getting  their 
proper  amount  of  diastolic  rest,  and  that  we  have  almost 
certainly  to  deal  with  a  severe  affection  of  the  cardiac 
muscle — cardiac  muscle  failure,  either  temporary  or 
permanent — and  effective  measures  of  treatment  must 
be  undertaken  at  once.  An  invariable  symptom  in  true 
bruit  de  galop  is  dyspnoea  on  slight  exertion. 


IV 
HEART   MURMURS 

Hitherto  we  have  been  considering  conditions  in  which 
the  vdlve  curtains,  even  if  altered  structurally,  have 
beeu  able  to  meet  properly  and  to  competently  obliterate 
the  orifice  they  guard  with  or  without  modification  of 
the  normal  sound  produced  by  the  closure  of  the  valve. 
The  valve  also  has  offered  no  resistance  to  the  passage 
of  blood  through  it  in  the  normal  direction  of  flow 
through  the  heart. 

MupmuPS. — In  disease,  however,  it  frequently  happens 
that  the  valve  is  so  changed  that  it  either  ohstructs  the 
flow  of  blood  in  the  normal  direction  through  the  heart 
or  allows  the  blood  to  pass  back  in  the  wrong  direction 
(to  regurgitate),  setting  up  sound-producing  vibrations 
in  the  blood  itself  or  in  the  valve  curtains,  or  in  both,  and 
giving  rise  to  new  or  adventitious  signs — "  murmurs  " 
or  "  bruits  " — instead  of,  or  in  addition  to,  the  ordinary 
sounds,  and  these  are  heard  over  the  heart. 

Timing  of  murmurs. — In  determining  the  valve  at 
which  a  murmur  is  caused,  it  is  essential  to  know  the 
phase  of  the  cardiac  cycle  during  which  tlie  murmur  is 
produced. 

It  is  of  the  utmost  importance  to  time  all  murmurs,  for 
by  so  doing  inexcusable  and  serious  errors  in  diagnosis 

48 


HEART   MURMURS  41J 

are  avoided.  It  is  often  impossible  to  feel  any  apex- 
beat,  or,  when  it  is  possible,  we  may  want  to  place  a 
stethoscope  over  it  Therefore,  the  best  way  to  time  a 
murmur  is  to  keep  a  thumb  on  the  carotid  pulse,  which 
follows  0'05  second  after  the  onset  of  v.s. 

One-twentieth  of  a  second  is  inappreciable  to  the 
ordinary  observer,  but  the  radial  pulse  is  O'l  second  after 
the  carotid  pulse,  and  this  is  appreciable  ;  for  instance, 
the  crescendo  murmur,  as  a  rule,  is  not  more  than 
O'l  second  in  duration. 

We   may  say  again  here  that  any  niuruiur  which  is 


Flo.  8.  — AiisoMiTE  Stenosis  OF  Fig.    9.— Absolutk     Stenosis 

Semilunar  Valve  THJiouiiH  of   Mitual  Valve  through 

TliICKENIX(J   OF    CUII'I'AINS    OF  THICKENING     AND     ADHESION 

Valve  :  Vkutical  Section.  of  Cusrs  of  Valve  Cuktains  : 

Viewed  Transversely. 

synchronous  with  the  carotid  pulse  is  v.s.  in  rhythm, 
and  any  one  not  syncronous  is  v.d.  in  rhythm.  The  a.v. 
crescendo  murmur  is  an  exception  to  this  rule  (see  p.  79). 

Changes  in  the  Valves  which  lead  to  the  Pkoduction 

OF  Murmurs. 

Broadly  speaking,  these  changes  result  in  the  valves 
becoming  obstructive  or  incompetent. 

1.  Valvular  obstruction. — ^Through  thickening  of  the 
curtains  the  lumen  of  the  valve  is  diminished,  causing 
obstruction  to  the  free  passage  of  blood  through  it  in 
the  normal  direction  of  the  circulation  (Figs.  8  and  9). 


50  HEART   DISEASE 

In  most  of  these  cases  of  obstruction  there  is  a  greater 
or  less  degree  of  adhesion  of  the  curtains  to  each  other 
where  they  arise  from  the  fibrous  ring  of  the  valve  which 
correspondingly  diminishes  the  free-way,  and  causes  the 
condition  known  as  valvular  stenosis,  and  generally,  but 
not  always,  a  murmur  of  obstruction. 

Valvular  stenosis  may  be  actual  or  relative. 

Actual  stenosis  is  the  term  applied  Avhen  the  valve 
orifice  and  its  fair-way  is  actually  narrowed  by  disease. 

Relative  stenosis  is  the  term  applied  when  the  lumen 
of   the  valve  remains  normalj  but  the  cavity  beyond  it, 


Fig.  10. — Relative  Stenosis  of  Fig.   11. — Dilatation   of  a.-v. 

Semilunar  Valve,   Akteiiy  Valve  Ring:  Normal  Cuu 

T.EINO    dilated  :    VaLVE   OrI-  TAINS        UNABLE        TO       MEET 

FICE   NOIIMAL    IN    SiZE.  ACROSS  THE  DiLATED  OrIFICE. 

into  which  the  blood  passes  from  the  valve,  is  abnormally 
large  or  dilated.  Such  a  condition  is  only  met  with 
practically  in  connection  with  the  semilunar  valves  and 
the  aorta  and  pulmonary  artery  beyond  them  (Fig.  10). 
A  stenosed  valve,  actual  or  relative,  may,  but  does  not 
always,  cause  a  murmur  during  the  passage  of  blood 
through  it  in  the  normal  direction  of  flow  through  the 
heart. 

2.  Valvular  incompetence. — Here  the  curtains  are 
unable  to  prevent  regurgitation  of  blood  through  the 
valve   in   the   opposite   direction   to  that  of  the  normal 


HEART  MURMURS  51 

course  through  the  heart,  and  during  this  regurgitation 
a  murmur  is  heard. 

Such  incompetence  may  arise  in  two  ways  : 

(1)  The  valve  curtains  are  normal j  but  the  orifice  is 
dilated — that  is,  the  area  of  the  orifice  is  rendered 
abnormally  great  through  stretching  of  the  structures 
which  normally  limit  it.  This  condition  is  met  with 
chiefly  in  stretching  of  the  circular  muscular  fibres 
around  the  orifices  of  the  a.-v.  valves  (Fig.  11). 

(2)  The  valve  curtains  are  diseased  and  unable  to  meet 
competently  across  the  orifice  of  a  valve,  which,  as  the 
result  of  the  disease,  is  generally  of  diminished  lumen, 
or  actually  stenosed  (see  Figs.  8  and  9). 

Failure  of  the  circular  muscular  fibres  may  be  present 
along  with  disease  of  the  valve  curtains. 

Murmurs  then  can  arise  through — 

{a)  Ohstruction  to  the  normal  fiow  of  the  blood  through 
the  heart;  or 

{}))  Incompetence  of  a  valve  to  prevent  the  regurgitation 
of  blood  in  the  reverse  direction  to  the  normal  flow. 

The  Physical  Causes  op  Cardiac  Murmues. 

There  are  two  chief  physical  causes  of  cardiac  murmurs 
— fluid  veins  and  vibration  of  valve  curtains.  Changes 
in  the  viscosity  of  the  blood  also  may  have  some  in- 
fluence. 

1.  Fluid  veins. — When  a  stream  of  blood  is  driven 
through  an  orifice  which  is  of  relatively  small  area  com- 
pared with  that  of  the  mass  of  blood  into  which  it  passes, 
sound-producing  currents,  or  eddies  of  blood,  are  pro- 
duced which  are  more  intense  when  there  is  a  greater 
disproportion  between  the  moving  column  and  the  mass 


52  HEART   DISEASE 

into  which  it  passes  and  when  the  driving  force  is 
increased. 

Such  a  method  of  producing  a  murmur  can  l)e  imi- 
tated by  blowing  through  the  pursed-up  lips,  the  lips 
remainino'  ri"'id. 

For  the  development  of  a  fluid  vein  it  is  necessary  that 
some  degree  of  -stenosis,  absolute  or  relative,  should  exist. 

(a)  In  Absolute  Stenosis  there  is  an  actual  narrowing 
of  the  valve  orifice  with  the  cavity  beyond  (that  is,  in 
relation  to  the  direction  of  the  stream  of  blood  causing 
the  murmur)  of  normal  or  abnormal  size. 

The  most  typical  conditions  in  which  this  absolute 
stenosis  is  met  with  are  those  of  mitral  and  aortic 
stenosis.  In  these  conditions  the  valve  orifice  is  more 
or  less  narrowed  by  adhesion  of  the  cusps  of  the  valves, 
with  some  thickening  of  the  non-adherent  portions  of  the 
valves  (see  Figs.  8,  9,  and  12). 

Tricuspid  and  pulmonary  stenosis  also  occur,  though 
not  so  commonly. 

(Ij)  In  Relative  Stenosis  the  valve  orifice  remains 
normal  in  area  and  the  cavity  beyond  is  pathologically 
dilated.  It  occurs  only  at  the  aortic  and  pulmonary 
valves.  Theoretically,  it  might  occur  at  the  a.-v.  valves 
if  the  ventricles  be  much  dilated,  and  so  account  for  rare 
a.-v.  diastolic  murmurs  heard  in  cardiac  dilatation.  But 
in  practice  relative  stenosis  is  only  important  at  the 
semilunar  valves. 

The  fluid  vein  murmur  is  of  a  smooth,  soft,  blowing 
character,  and  probably  not  transmitted  as  widely  as 
when  there  is  valve  vibration  as  well. 

Stenosed  valves  are  also  often  incompetent  as  well  as 
obstructive,  when  regurgitation  of  blood  through  the 
narrow  opening  will  cause  a  murmur  of  fluid-vein  origin, 
and  probably  also  of  valvular  vibration  origin. 


HEART  MURMURS  53 

It  must  be  remeriib(3red  tlitit  vvlieri  there  is  obstruction 
to  the  flow  of  blood  through  a  valve,  the  cavity  of  the 
heart  behind  the  valve  (in  relation  to  the  normal  direction 
of  blood-flow)  is  often  imperfectly  emptied,  and  therefore 
contains  blood  for  the  development  of  a  fluid-vein  re- 
gurgitant murmur. 

It  must  also  be  borne  in  mind  that  the  curtains  of  a 
valve  which  adhere  to  each  other  and  cause  absolute 
stenosis  may  be  thrown  into  vibration  by  the  stream  of 
blood  and  alter  the  character  of  the  murmur  [see  next 
subheading  (2)]. 

2.  Vibration  of  the  valve  curtains.— (1)  Ohstruction 
murmurs  may  be  produced  by  the  blood  throwing  the 
rough,  stiffened  curtains  into  sound-producing  vibration 
as  it  passes  over  them  in  its  direct  passage  through  the 
heart. 

(2)  The  regurgitation  of  hlood  over  similarly  diseased 
curtains  throws  them  into  vibration  and  produces  a 
murmur. 

Tj-ie  sound-producing  vibration  of  the  valve  thus  caused 
is  analogous  to  that  of  a  flag  fluttering  in  the  wind. 

Vibration  murmurs  are  of  a  rougher,  more  vibratory 
character  than  those  produced  by  a  fluid  vein. 

Not  uncommonly  a  tag  of  fibrous  tissue  attached  to  a 
valve  is  thrown  into  rapid  vibrati  »n  by  the  blood-stream, 
and  produces  a  musical  murmur  without  causing  any 
symptoms  of  heart  disease ;  and  it  may  be  pointed  out 
here  that  the  loudness  of  any  cardiac  rnurmur  is  not 
necessarily  an  indication  of  the  severity  of  the  lesion, 
the  "  bark  '^  of  a  murmur  often  being  worse  than  its 
''  bite.'' 

N.B. — It  is  the  condition  of  the  cardiac  muscle,  not 
of  the  valve,  that  determines  prognosis. 


54  HEART   DISEASE 

Thrills, — In  marked  cases  we  can  feel  the  vibration 
murmur  as  a  "thrill/'  typical  instances  of  which  are 
the  thrills  met  with  frequently  in  mitral  and  aortic 
stenosis. 

3.  Murmurs  due  to  chang-es  in  the  blood — Haemic 
murmurs. — In  marked  cases  of  ana3mia  a  systolic  mur- 
mur, usually  called  a  "  haemic  murmur/'  is  frequently 
heard  over  the  heart,  with  its  point  of  maximum  intensity 
generally  in  the  pulmonary  valve  region. 

It  used  to  be  thought  that  the  actual  blood  change — 
namely,  the  diminished  number  of  red  corpuscles  per 
cm.,  especially  if  the  total  blood  volume  be  abnormally 
great,  as  in  chlorosis — gave  rise  to  the  sound.  There  is, 
however,  no  satisfactory  proof  that  endocardial  murmurs 
can  arise  as  a  consequence  of  diminished  viscosity.  They 
are  probably  of  valvular  origin,  and  arise  in  one  of 
two  ways : 

(1)  Begurgitation  through  the  mitral  valve,  which  has 
been  rendered  incompetent  by  the  circular  muscular 
fibres  of  the  valve  partaking  in  the  condition  of  ven- 
tricular weakness  not  uncommonly  met  with  in  severe 
anasmia;  in  other  words,  mitral  incompetence  through 
valvular  dilatation,  the  curtains  remaining  normal.  This 
murmur  is  best  heard  at  the  apex  of  the  heart. 

(2)  III  relative  stenosis  of  the  pulmonary  valve,  which 
is  brought  about  by  dilatation  of  the  artery  in  its  first 
part  immediately  beyond  the  valve,  the  valve  orifice 
remaining  normal.  Such  a  condition  of  dilatation  can 
be  made  out  in  the  post-mortem  room.  This  murmur 
is  best  heard  over  the  region  of  the  pulmonary  valve. 

iV.jC?. — Murmurs  caused  in  the  above-mentioned  ways 
are  all  diminuendo  in  character,  dying  aicay  with  the  force 
which  jyToduces  them. 


11 K ART   MURMUR 8  55 

Changes  in  the  Different  Valves  wiircii  (Iive  Rise 

TO  Murmurs. 

It  will  make  things  clearer  if  the  changes  in  the 
different  valves  which  give  rise  to  murmurs  be  now 
considered. 

1.  Auriculo-ventricular  valves — («)  Actual  stenosis. 

— This  results  from  thickening  and  adhesion  of  the  valve 
curtains,  which  consequently  oppose  the  passage  of 
blood  from  auricle  to  ventricle  ;  and  if  the  forces  moving 
the  blood,  especially  that  of  auricular  systole,  are  strong 
enough,  which  is  not  always  the  case,  a  diastolic  murmur 
will  be  heard.     Sometimes  vibrations  are  thus  produced 


Fig    12. — Two  Dkgrke.s  of  Adhesion  of  Mitral  Cuktaiks 
CAUSING  Stenosis. 

in  the  valve  curtains,  and  these  can  be  palpated  at  the 
apex  as  a  diastolic  thrill. 

The  degree  of  stenosis  varies,  and  may  be  so  extreme 
as  to  narrow  the  orifice  of  the  valve  from  an  area 
admitting  three  finger-tips  to  one  scarcely  admitting  the 
tip  of  the  little  finger  only — the  so-called  button-hole 
orifice  (see  Figs.  9  and  12). 

The  musculi  papillares  and  chordae  tendineae  participate 
more  or  less  in  this  thickening  and  rigidity,  and  may  in 
consequence  fix  the  edges  of  the  valve  curtains  in  a 
funnel-shaped  structure,  and  prevent  the  normal  move- 
ments and  co-aptation  of  the  curtains  during  v.fi. 


56  HEAET   DISEASE 

The  process  which  causes  this  sclerosis  is  generally 
of  a  chronic,  slowly  progressing  nature,  mostly  set  up 
in  childhood,  and  often  without  symptoms  to  attract 
attention. 

As  a  result  of  these  changes  the  valve,  in  addition  to 
being  obstructive,  is  very  often  incompetent,  allows  oi 
reguryitafion,  and  creates  a  systolic  murmur  during  v.s. 

The  presence  of  vegetations  on  the  valves  without 
adhesion,  which  occurs  in  acute  endocarditis,  will  ob- 
struct the  flow  of  blood  from  the  auricle  to  the  ventricle, 
and    may   cause    a    diastolic   murmur.     They  generally 


FfG.  13. — Vegetations  ox  ]\1itral  Vai.ve  (closed)  which  prevent 
Competent  Closuiie,  and  which  obstruct  tjie  Flow  of  Blood 
through  the  Open  Valve. 

There  is  no  adhesion  of  the  curtains  and  no  true  stenosis. 

make  the  valve  incompetent,  and  give  rise  to  a  .systolic 
murmur  of  regurgitation. 

Confusion  of  terms.' — The  terms  ohstrudion  and 
stenosis  (referring  here  to  actual,  not  relative  stenosis) 
are  often  rather  loosely  used  as  meaning  the  same  condi- 
tion of  a  valve.  Whilst  all  forms  of  absolute  stenosis 
obstruct  the  flow  of  blood  throuo-h  the  valve,  a  condition 
may  occur  in  which,  through  marked  roughening  or  the 
presence  of  vegetations  on  the  curtains  without  adhesion 
of  the  curtains,  the  normally  unhindered  flow  of  blood 
through  a  valve  may  be  obstructed  and  an  a.-v.  diastolic 
murmur  result  (see  Fig.  13). 


HEART   MURMURS  57 

The  latter  condition  would  be  really  one  of  obstruc- 
tion, but  hardly  one  of  absolute  stenosis,  this  term 
generally  implying*  absolute  narrowing  of  the  blood-way 
through  the  valve  caused  by  adhesion  of  the  curtains  or 
nodular  excrescences  stiffening  the  valves 

{h)  Valvular  dilatation. — Here  the  deficient  factor  in 
the  closure  of  the  valve  is  the  inability  of  the  muscular 
fibres  round  the  valve  ring  to  reduce  the  orifice  of  the 
valve  during  v.s.  to  an  area  which  the  curtains,  remain- 
ing normal,  can  competently  close.  In  consequence,  a 
systolic  murmur  of  regurgitation  is  caused  during  v.s. 
This  condition  results  from  cardiac  muscle  failure  (see 
Fig.  11). 

The  musculi  papillares  may  also  be  unable  to  contract 
and  hold  the  edges  of  the  curtains  down.  In  this  case 
the  curtains  bulge  into  the  auricle  and  probably  become 
incompetent. 

(a)  and  [h). — As  the  result  of  acute  endocarditis  the 
valve  curtains  may  become  affected  with  vegetations, 
which  impede  the  flow  of  blood  from  auricle  to  ven- 
tricle and  prevent  competent  closure  of  the  valve  during 
ventricular  systole  ;  and  at  the  same  time  the  muscle 
element  of  the  valve  may,  as  a  result  of  coincident  myo- 
carditis, fail  and  cause  enlargement  of  the  ring  of  the 
valve.  In  such  a  condition  a  systolic  murmur  is  almost 
certain  to  be  heard,  and  possibly  a  diastolic  murmur 
also. 

Cardiac  dilatation  with  no  murmur, — It  must  be 
noted  that  cardiac  muscle  failure,  leading  to  dilatation 
of  the  heart,  may  occur,  and  yet  no  systolic  murmur 
of  valvular  incompetence  be  heard.  In  these  cases  the 
circular   and   spiral   muscular   fibres  of   the   valve   ring 


58  HEART   DISEASE 

must  be  more  resistant  to  stress  and  strain  than  the  rest 
of  the  ventricular  muscle,  and  are  not  stretched  at  all,  or 
only  to  a  slight  degree  which  the  valve  curtains  can 
make  good  and  so  prevent  regurgitation.  We  shall  then 
have  no  systolic  murmur  of  regurgitation,  only  an 
accentuated  or  reduplicated  fij-st  sound. 

Ulcerative  erosion  of  curtains. — Valvular  incompe- 
tence may  result  from  ulcerative  endocarditis  eroding 
holes  through  the  valve  curtains  and  thus  allowing  of 
regurgitation;  but  such  a  condition  would  be  impossible 
to  recognize  clinically.  It  would  probably  occur  with 
changes  in  the  edges  of  the  valve  curtains,  which  would 
themselves  create  incompetence. 

2.  Semilunar  valves. — The  changes  which  lead  to 
valvular  murmurs  at  the  aortic  and  pulmonary  orifices 
are  practically  the  same  as  those  above  described  at  the 
a.-v.  valves,  with  the  difference  that  there  are  no  musculi 
papillares  and  practically  no  muscular  or  elastic  element 
in  the  valve  ring.  The  rhythm  of  the  murmurs  is,  how- 
ever, different.  Thus,  at  a  stenosed  semilunar  valve  the 
obstructive  murmur  is  systolic  in  rhythm  and  the 
regurgitant  murmur  diastolic,  whilst  at  a  stenosed 
auriculo-ventricular  orifice  the  obstructive  murmur  is 
diastolic  and  the  regurgitant  systolic. 

The  aortic  obstructive  murmur,  being  always  caused 
by  the  great  force  of  ventricular  systole,  is  much  more 
regularly  heard  than  the  mitral  obstructive  murmur. 
The  obstructive  aortic  murmur  may  be  accompanied 
by  a  thrill  palpable  over  the  aortic  area. 

N.B. — A  systolic  murmitr  at  the  auriculo-ventricular 
valves,  or  a  diastolic  inurinur  at  the  semilunar  valves, 
per  se,  only  means  incompetence  of    these  valves.     The 


HEART   MURMURS  59 

rhytlim  of  these  )tiitrmws  gives  no  information  whatever 
rr-v  to  the  caicse  of  the  incompetence — that  is,  whether  this 
is  due  to  stenosis  or  dilatation.  The  means  of  deter- 
mining this  point  will  be  referred  to  later. 

The  Crescendo  mupmup. — So  far  we  have  dealt  with 
murmurs  which,  however  they  may  be  caused,  have  a 
common  feature — namely,  they  are  diminuendo  in  char- 
acter, and  die  away  with  the  force  which  creates  them. 

There  is,  however,  another  murmur  which,  instead  of 
dying  away,  increases  in  force  until  it  is  abruptly  cut 
short  at  its  maximum  intensity  by  an  accentuated  first 
sound.  It  is  therefore  a  crescendo  murmur.  In  addition 
to  this,  it  has  another  essential  characteristic — namely, 
it  rises  in  pitch  progressively  with  its  increase  in  vigour, 
and  is  at  its  highest  pitch  and  maximum  force  when  it  is 
abruptly  terminated  by  the  accentuated  first  sound. 

This  t3^pe  of  murmur  is  only  produced  at  a  stenosed 
auriculo-ventricular  valve,  and  almost  always  at  the 
mitral  valve.  A  tricuspid  crescendo  murmur  is  very 
rare.  A  crescendo  murmur,  then,  has  three  essential 
features : 

(1)  Increasing  force,  (2)  Bising  pitch,  and  (3)  Abrupt 
termination  hy  an  accentuated  first  sound  at  its  maximuin 
of  force  and  highest  pitch. 

Such  a  murmur,  except  the  terminal  abrupt  first  sound, 
can  be  imitated  closely  by  blowing,  with  increasing  force, 
through  the  lips  pursed  up  to  produce  a  low-pitched 
whistling  sound,  and  closing  the  lips  whilst  doing  this. 
In  this  way  the  sound  represented  by  oo-ip  is  created. 
It  can  also  be  imitated  by  blowing  through  a  piece  of 
drainage  tubing  and  obliterating  the  lumen  of  the  tube 
with  the  fingers  or  teeth  whilst  doing  so.  The  rising 
pitch  characteristic  of  the  murmur  can  only  be  caused 


60  HEART  DISEASE 

afc  an  orifice  Avliich  is  he Ing  progressively  closed  during 
the  prodicction  of  the  murmur. 

Causation  of  the  Crescendo  murmur. — It  is  usually 
taught  that  this  crescendo  murmur  is  caused  immedi- 
ately before  the  onset  of  c.s-.  by  systole  of  the  auricle_, 
and  therefore  it  is  called  a  presystolic  or  auricular 
systolic  murmur.  The  auricle  is  .  supposed  to  contract 
with  a  crescendo  force^  and  to  terminate  its  contraction 
abruptly  at  its  maximum  of  effort.  During  this  con- 
traction blood  is  forced  through  the  stenosed  mitral 
valve  and  produces  the  murmur.     How  the  rising  pitch 


Fig.  14. 

A,  B,  C,  D,  Progressive  stages  ia  the  obliteration  of  the  lumen  of  a 
tube  in  which  is  being  produced  an  imitation  crescendo  murmur  ; 
E,  F,  condition  of  the  lumen  of  the  tube  when  a  systolic  murmur 
continues  ihe  crescendo  murmur, 

characteristic  of  the  murmur  is  imparted  to  it  during 
a.s.  has  never  been  explained.  This,  as  I  have  said, 
must  be  produced  at  an  orifice  which  progressively 
closes  whilst  a  murmur  is  being  produced  at  it ;  and 
how  the  auricle  can  at  one  and  the  same  time  keep  open 
and  yet  progressively  close  the  stenosed  valve  by  driving 
blood  through  it  has  never  been  explained. 

The  Crescendo  murmur  is  early  ventricular  systolic 
in  rhythm.  The  a.-v.  crescendo  murmur  must,  in  my 
opinion,  be  produced  between  the  onset  of  v.s.  and  the 
carotid  pulse  ;  that  is,  be  early  v.s.  or  prespliygmi-c  in 
rhythm. 


HEART   MURMURS  61 

The  accentujited  first  sound  which  terminates  the 
crescendo  murmur  is  probably  caused  by  the  forcible 
coaptation  of  the  thickened  margins  of  the  valve,  and 
must  be  ])roduced  at  a  later  phase  of  v.s.  than  the 
normal  first  sound.  This  view  of  the  early  ventricular 
or  presphygmic  rhythm  of  the  a. -v.  crescendo  murmur, 
and  the  lateness  of  the  first  sound  which  terminates  it, 
has  been  supported  by  independent  observers  with 
evidence  obtained  by  accurate  timing  of  the  events  of 
the  cardiac  cycle  in  mitral  stenosis  with  instruments 
recording  synchronously  tracings  of  the  carotid  pulse 
and  of  the  heart  sounds. 

Semilunar  valve  cre.srendo  mitrmiir. — Theoretically,  a 
crescendo  murmur  may  be  caused  at  a  diseased  semi- 
lunar valve,  with  curtains  which  are  not  as  mobile  as 
the  normal  ones,  but  require  some  greater  force  than 
the  cessation  of  the  vis  a  teryo  of  ventricular  systole  to. 
close  them.  This  might  be  developed  at  a  later  phase 
of  ventricular  diastole  than  that  at  which  the  normal 
semilunar  valves  close,  by  "  systole  "  of  the  artery,  and 
whilst  the  valves  were  being  closed  blood  would  re- 
gurgitate through  their  gradually  narrowing  orifice  and 
create  a  murmur  of  rising  pitch.  It  is  very  probable 
that  the  short  aortic  diastolic  "  whiffs  '^  are  caused  in 
this  way. 

Murmurs  accompanying  heart  sounds  produced  at 
the  same  phase  of  the  ventricular  cycle. — Sometimes  a 
murmur  is  accompanied  by  a  heart  sound  produced 
during  the  same  phase  of  the  ventricular  cycle.  Why 
this  should  be  so  is  not  always  clear. 

It  is  easy  to  understand  how  a  first  sound  produced  at 
the  a.-v.  valves  can  accompany  a  systolic  murmur  pro- 
duced at  the  semilunar  valves,  or  if  the  a.-v.  valves  give 


62  HEART   DISEASE 

rise  to  a  diastolic  murmur,  and  the  semilunar  valves  are 
normal,  a  second  sound  will  be  heard  with  the  murmur. 
Difficulties  arise,  however,  when  both  the  sound  and 
murmur  are   produced   at  one   of   the  pairs  of  a.-v.  or 
semilunar  valves.      Such  an  occurrence  may  be  due — 

1.  To  the  mitral  (or  the  aortic)  valve  being  so  affected 
as  to  create  a  murmur  of  regurgitation  but  no  sound, 
the  tricuspid  (or  the  pulmonary)  valve  curtains  respec- 
tively remaining  normal  and  producing  an  audible 
sound ;  or  vice  versa  to  the  tricuspid  (or  pulmonary) 
valve  allowing  regurgitation,  the  mitral  (or  aortic)  valve 
remaining  normal  and  producing  a  sound  which  is 
audible  through  the  murmur. 

2.  To  the  curtains  of  one  affected  valve  being  in  such 
a  condition  that  they  can  close  with  a  sound  and  yet  not 
be  sufficiently  competent  to  prevent  some  regurgitation 
and  the  development  of  a  murmur  after  the  sound.  This 
condition  may  be  met  with  in  incompetence  from  stenosis 
or  dilatation.  When  the  murmur  and  sound  arise  at  the 
same  valve  during  the  same  phase  of  the  ventricular 
cycle  the  murmur  distinctly  follows  the  sound.  There 
is  one  exception  to  this,  namely,  the  crescendo  murmur 
which  precedes  the  first  sound,  both  murmur  and  sound 
being  caused  by  v.s.  (p.  60). 

Absence  of  sounds  with  apparently  normal  rigrht 
heart  valves. — It  not  uncommonly  happens  that  where 
there  is  apparently  disease  of  only  the  mitral  or  the  aortic 
valves,  and  not  of  the  right  side  valves,  the  murmur 
produced  at  the  diseased  valve  is  often  unaccompanied 
by  any  normal  sound  which  ought  to  have  been  produced 
at  the  corresponding  healthy  valve.  Thus  in  cases  with 
incompetence  of  an  abnormal  mitral  valve,  and  an  ap- 
parently normal   tricuspid  valve,  a  systolic  murmur  of 


HEART   MURMURS  63 

mitral  regurgitation  may  be  heard,  with  no  tricuspid  first 
sound.  Or_,  again,  in  aortic  incompetence,  and  apparently 
a  normal  pulmonary  valve,  a  diastolic  aortic  murmur  is 
not  infrequently  heard  with  no  pulmonary  second  sound. 
These  facts  may  mean  either  that  the  tricuspid  or  the 
pulmonary  valve  is  unable  to  produce  a  first  sound  of  its 
own,  which  is  contrary  to  common  belief,  or  that  the  first 
and  second  sounds  produced  at  the  normal  right  side  of 
the  heart  have  not  sufficient  intensity  to  be  heard  through 
a  murmur. 

Incompetence  through  dilatation  of  a  valve, — It  is 

interesting  to  consider  why,  if  the  curtains  of  an  a.-v. 
valve  are  normal,  but  through  dilatation  of  the  orifice 
a  murmur  is  produced,  there  is  not  always  a  sound  of 
tension  also.  There  often  is,  but  not  uncommonly  it 
happens  that  a  soft  systolic  murmur  of  muscle-failure 
incompetence  is  heard  with  no  first  sound.  This  may 
be  explained  in  one  of  several  wa3^s  : 

1.  In  a  normal  heart  the  a.-v.  curtains  are  "floated" 
up  into  apposition  by  the  filling  of  the  ventricle ;  then — 

2.  At  the  very  onset  of  v.s.  they  are  competently 
locked,  and  this  provides  the  resistance  for  the  "ex- 
plosive" contraction  of  the  ventricle,  which  throws  the 
curtains  into  sound-producing  tension,  and  also  causes 
a  note  of  muscle  contraction. 

3.  If  the  valve  curtains  are  unable  to  meet  across  a 
dilated  orifice  they  cannot  be  competently  locked  at  all 
by  V.S.,  but  allow  blood  to  slip  away  and  so  prevent  the 
necessary  resistance  for  the  normal  explosive  contraction 
of  the  ventricle  and  its  sound-producing  (curtain  and 
muscle  tension)  results.  The  more  gradual  tension  of  the 
curtain  and  muscle  fails  to  produce  a  first  sound,  a 
murmur  taking  its  place.     In  support  of  this  contention 


64  HEART   DISEASE 

is  the  fact  that  a  systolic  murmur  sometimes  grows  in 
intensity  pari  passu  with  the  abnormally  slow  develop- 
ment of  the  maximum  of  v.s. 

Influence  of  mobility  of  curtains  on  sounds. — 

(a)  Mitral  and  tricuspid  valves. — It  does  not  follow, 
then,  that  Avhen  a  systolic  murmur  of  regurgitation  is 
heard  the  absence  of  a  first  sound  denotes  loss  of  mobility 
of  the  mitral  or  tricuspid  [a. -v.)  valve  curtains. 

(h)  Aortic  and  pulmonary  valves. — Absence  of  a  second 
sound  when  an  aortic  or  pulmonary  murmur  of  regurgita- 
tion is  heard  does  mean  almost  certainly  loss  of  mobility 
(atheroma)  of  the  valve  curtains.  This  is  probably  ex- 
plained by  the  fact  that  the  normal  semilunar  valve 
curtains  are  thrown  more  suddenly  into  tension  by  the 
pressure  in  the  large  arteries,  which  is  at  its  maximum 
at  its  onset,  than  are  the  a. -v.  valves  by  the  slower-acting 
muscle  of  the  ventricles.  A  leak  in  the  semilunar  valve 
will,  then,  not  have  the  same  effect  on  the  development 
of  sound-producing  tension  in  them  as  will  a  leak  in  the 
a.-v.  valves. 

The  presence  or  absence  of  a  second  sound  with  an 
aortic  (or  pulmonary)  incompetent  murmur,  therefore, 
gives  more  information  as  to  the  mobility  of  the  valve 
curtains  than  is  the  case  with  a  similar  condition  at  the 
a.-v.  valve. 


V 

AREAS    OF  AUDIBILITY   OF   HEART 

MURMURS 

Situation  of  the  valves. — Broadly  speaking,  the  mur- 
murs produced  at  the  various  valves  of  the  heart  are 


Fig.  15. 

A.,  Aorta  ;  A.V.,  aortic  valve  ;  M.,  mitral  valve  ;  P. A.,  pulmonary  artery  ;  P.V.,  pul- 
monary valve  ;  R.A.,  right  auricle  ;  SF.,  septum  ventriculorum  ;  S.V.C,  superior 
vena  cava  ;   7".  F.,  tricuspid  valve.     (Cunningham.) 

heard    best  at    those    parts   of    the   anterior  chest-wall 
Avhich   are   named    after   the   individual  valves.     These 

65  5 


66  HEART  DISEASE 

areas  are  not  all  directly  over  the  valves,  the  situation 
of  which  may  be  stated  accurately  enough  for  all  prac- 
tical purposes  to  be  as  follows  :  Pulmonary  valve  at  the 
level  of  the  third  left  costal  cartilage ;  aortic  valve,  third 
interspace ;  mitral  valve,  fourth  costal  cartilage ;  and 
tricuspid  valve,  fourth  interspace,  and  in  a  line  running 
obliquely  downwards  from  the  third  left  cartilage,  where 
it  joins  the  sternum,  to  the  midsternal  line  at  the  level 
of  the  sixth  rib. 

Mitral  area. — Murmurs  produced  at  the  mitral  valve 
are  best  heard  at  the  apex  of  the  left  ventricle — i.e.,  the 
apex-beat  in  the  fifth  interspace  f  inch  internal  to  the 
mid-clavicular  line,  or  3  J  inches  from  the  midsternal  line. 

If  the  heart  is  enlarged  or  displaced,  the  apex  must 
be  located  as  accurately  as  possible  in  its  new  situation 
by  the  methods  described  previously. 

The  danger  of  using  the  ni'pjple  as  a  landmarh  must  be 
remembered.  Thus  it  may  be  out  of  place  in  relation  to 
the  midsternal  line  through  abnormalities  in  the  shape 
of  the  chest,  and  in  women,  naturally,  it  is  generally  no 
guide  at  all. 

Tricuspid  area. — Tricuspid  murmurs  are  heard  best 
at,  and  to  the  left  of,  the  lowest  part  of  the  body  of  the 
sternum. 

Aortic  area. — The  area  at  which  experience  shows 
aortic  systolic  murmurs  to  be  generally  best  heard  is  that 
of  the  first  intercostal  space  against  the  sternum,  behind 
the  second  right  costal  cartilage  at  its  junction  with  the 
sternum,  or  on  the  sternum  at  this  level.  This  is  where 
the  arch  of  the  aorta  comes  nearest  to  the  anterior  chest- 
wall,  and  sounds  produced  at  the  aortic  orifice  during 
systole  of  the  ventricle  are  conducted  along  the  aorta. 


EFFECT  OF  POSTURE  ON  MURMURS  67 

Diastolic  aortic  murmtcrs,  however,  may  be  inaudible 
here,  and  are  generally  heard  best  down  the  left  margin 
of  the  sternum  or  over  the  tricuspid  area.  They  may 
be  audible  at  any  small  area  of  the  pra3cordia  only ;  so 
an  aortic  diastolic  murmur,  when  suspected,  must  be 
sought  for  carefully,  square  inch  by  square  inch,  all  over 
the  chest  anterior  to  both  ventricles. 

Pulmonary  area. — The  pulmonary  area  is  situated 
at  the  junction  of  the  third  left  costal  cartilage  and 
sternum,  or  in  the  third  left  intercostal  space  against 
the  sternum. 

Whilst  the  above-mentioned  principles  relating  to  the 
area  of  audibility  of  murmurs  produced  at  the  different 
valves  hold  good  in  most  cases,  it  must  be  remembered 
that  a  murmur  produced  at  any  one  of  the  orifices,  if 
intense  enough,  may  he  heard  all  over  the  'prsecordium 
(see  Section  YI.) . 

Effect  of  Change  feom  the  Upright  to  the  Lying 
Down  Position  on  Murmurs. 

It  is  important  to  note  that  some  organic  murmurs^ 
especially  mitral  systolic  murmurs,  are  most  marked  when 
the  patient  is  lying  down.  They  may,  indeed,  only  be 
heard  when  he  is  in  this  position,  so  in  doubtful  cases 
examination  in  the  erect  posture  only  is  not  conclusive. 


VI 

CONDUCTION  AND  TRANSMISSION 
OF  MURMURS 

Conduction  means  the  carrying  of  lieart  sounds  and 
murmurs  from  their  seat  of  origin  to  other  parts  of  the 
heart  (or  pr^ecordia)  and  into  the  large  vessels  by  means 
of  the  heart  muscle  or  the  blood. 

Transmission  means  the  carrying  of  the  sounds  and 
murmurs  beyond  these  limits  by  means  not  thoroughly 
understood. 

Conduction. — a  murmur  is  conducted  best  in  ttie 
direction  of  ttie  flow  of  blood  which  causes  it.    We  can 

get  fairly  close  with  our  stethoscopes  to  the  direction  of 
the  flow  of  blood  through  the  tricuspid,  pulmonary  and 
aortic  valves. 

The  tricuspid  and  pulmonary  valves,  being  on  the  right 
side  of  the  heart,  which  forms  the  anterior  and  most 
superficial  part  of  the  organ  as  it  lies  in  the  chest,  are 
nearer  to  the  anterior  portion  of  the  chest  than  are  the 
mitral  and  aortic  valves. 

1.  Tricuspid  murmurs.— A  systolic  murmur  ought  to 
be  conducted  towards  the  right  of  the  sternum,  the  right 
auricle,  especially  when  dilated,  extending  well  beyond 

68 


CONDUCTION  OF   MURMURS  69 

the  r'lQ-ht  border  of  the  sternum.     It  is  heard  over  the 

o 

praecordia  anterior  to  the  right  ventricle. 

A  diastolic  murmur  is  conducted  towards  the  apex  of 
the  right  ventricle. 

Both  murmurs  are  difficult  to  distinguish  from  mitral 
murmurs. 

2.  Pulmonary  murmurs.— The  pulmonary  artery  at 
the  base  of  the  right  ventricle  is  nearer  the  anterior  wall 
of  the  chest  than  the  aorta^  but  its  divisions  are  deeply 
seated  within  the  chest. 

Systolic  pulmonary  murmurs  are  audible  to  the  left  of 
the  sternum  in  the  second  intercostal  space. 

A  diastolic  pulmonary  murmur  is  rare^  but^  when  heard, 
may  be  conducted  down  the  sternum  or  over  the  right 
ventricle. 

Aortic  murmurs. — Systolic  murmurs  are  conducted 
upwards  into  the  large  arteries,  subclavian  and  carotid, 
and  therefore  these  murmurs  are  conducted  to  more 
accessible  regions  than  any  other  heart  murmur. 

When  being  sought  for  over  the  vessels  in  the  neck, 
care  must  be  taken  to  avoid  pressure  on  the  artery, 
otherwise  a  murmur  will  be  produced  from  the  pressure 
itself. 

They  may  be  easily  heard  over  the  apex-beat,  though 
less  distinctly  there,  as  a  rule,  than  at  the  aortic  area. 
When  traced  from  the  aortic  cartilage  to  the  apex- 
beat  over  the  pra3cordia  they  gradually  decrease  in 
loudness. 

Diastolic  murmurs  will  be  conducted  back  into  the 
left  ventricle,  and,  as  said  before,  may  be  audible  any- 
where over  that  part  of  the  chest-wall  lying  in  front  of 
both  the  ventricles.  Their  usual  line  of  conduction  is 
down  the   left  edge  of  the  sternum  below  the  level  of 


70  HEART    DISEASE 

the  aortic  area,  and  they   may  he  heard  at  the  tricuspid 
region  only. 

They  may  also  be  heard  over  the  sternum  towards  the 
pulmonar}^  area. 

Mitral  mupmuPS. — Systolic  murmurs  should  be  con- 
ducted towards  the  sternum  and  left  auricle,  but  the 
left  side  of  the  heart  is  too  deeply  situated  for  their 
conduction  to  be  traced.  They  may  be  transmitted  round 
through  the  axilla  to  the  back,  and  be  audible  at  the 
lowest  part  of  the  left  scapula. 

Diastolic  murmurs  are  best  heard  at  the  apex  of  the 
left  ventricle,  which  is  in  the  direction  of  the  flow  of 
blood  causing  them.  They  are  scarcely  ever  transmitted 
into  the  axillary  region. 

Crescendo  murmurs  are  audible,  as  a  rule,  only  over 
the  apex-beat,  but  they  are  occasionally  conducted  more 
or  less  widely  over  the  pr^cordia.  As  a  rule,  however, 
the  terminal  portion  or  accentuated  first  sound  only  is 
heard  away  from  the  apex  or  at  the  back. 

Transmission.— The  conditions  which  favour  the 
transmission  of  cardiac  murmurs  are  not  fully  under- 
stood; but  I  think  that  there  are  certain  factors  pre- 
disposing to  a  wider  area  of  audibility. 

1.  Condition  of  chest-wall. — A  thin  chest-wall,  with  no 
fat,  in  close  apposition  to  a  heart  without  intervening 
lung,  will  tend  to  favour  transmission.  Thus  a  largely 
dilated  heart  in  a  child  will  have  its  murmurs  trans- 
mitted more  widely  than  if  the  same  heart  were  in  an 
adult  with  thicker  or  more  rigid  chest-wall  and  more 
intervening  lung.  The  ribs  may  have  something  to  do 
with  transmission  of  mitral  murmurs,  especially  if  one 
be  immediately  in  contact  with  the  apex  of  the  heart. 


TRANSMISSION  OF   MURMURS  71 

2.  The  nature  of  the  murmur — that  is,  if  produced  by 
vihratioii  of  the  valve — will  have  some  effect.  In  my 
opinion,  such  a  murmur  will  be  conducted  and  trans- 
mitted more  widely  than  one  produced  by  the  small 
column  of  blood  passing  into  a  large  chamber  (fluid 
vein) . 

Thus  a  systolic  mitral  murmur  is  likely  to  be  trans- 
mitted further  through  the  axillary  region  if  it  is  pro- 
duced by  regurgitation  through  valve  curtains  distorted, 
thickened_,  and  made  nodular  by  chronic  endocarditis, 
and  capable  of  being  thrown  into  vibration  by  the  blood- 
stream, than  if  the  regurgitation  is  through  a  dilated 
orifice  with  normal  valve  curtains,  such  as  we  meet  with 
in  cardiac  muscle  failure,  or  through  a  rigid  thick  car- 
tilaginous funnel,  such  as  is  met  with  sometimes  in 
mitral  stenosis. 

But  loudf  vibratory  murmurs  are  not  always  conducted 
or  transmitted  the  farthest.  Thus,  I  have  several  times 
noticed  a  soft  systolic  murmur  produced  at  the  mitral 
or  aortic  orifice  which  was  audible  all  over  the  chest, 
and  even  down  over  the  lumbar  region  below  the  ribs. 
Several  of  these  cases  were  malignant  endocarditis,  with 
involvement,  especially,  of  the  aortic  cusp  of  the  mitral 
valve. 

Whilst  murmurs  produced  at  any  of  the  valves  may, 
if  intense  enough,  be  transmitted  in  the  opposite  direc- 
tion to  their  path  of  conduction,  those  produced  during 
systole  at  the  aortic  and  mitral  valves  are  the  mur- 
murs most  commonly  transmitted.  An  aortic  systolic 
murmur  is  frequently  transmitted  to  the  apex  of  the 
heart,  whilst  a  mitral  systolic  murmur  is  often  trans- 
mitted to  the  axillary  region. 


Vll 

SPECIAL  CHARACTERISTICS  OF  THE 

DIFFERENT   VALVULAR 

MURMURS 

MiTEAL  Murmurs. 

Lesions  of  the  mitral  valve  are  the  commonest  of  all 
valvular  lesions. 

Mitral  systolic  murmurs  vary  very  much  in  character 
according  to  the  condition  of  the  curtains  of  the  valve  at 
which  regurgitation  takes  place.  If  they  can  be  thrown 
into  vibration  by  the  regurgitant  stream  of  blood  the 
murmurs  are  more  intense,  harder^  rougher,  and  more 
penetrating  than  when  the  leak  is  between  normal 
curtains  which  are  incompetent  through  dilatation  of 
the  valve  orifice,  when  they  are  softer,  more  "  blowing," 
and  have  less  carrying  power.  A  projecting  tag  of 
fibrous  tissue  may  give  rise  to  a  loud  "  nmsical  "  murmur. 

The  murmur  is  of  uniform  pitch — that  is,  it  arises  at  a 
leak  which  is  constant  (in  relation  to  each  v.s.)  in  its 
area  whilst  the  murmur  is  being  produced.  In  intensity 
it  fades  with  the  cessation  of  v.s. — that  is, it  is  decrescendo. 
The  mitral  crescendo  murnmr  has  characteristics  peculiar 
to  itself. 

72 


MITRAL   MURMURS  73 

In  time  it  is  synchronous  with  the  throb  in  the  carotid 
artery.  The  murmur  may  or  may  not  be  accompanied 
by  a  first  sound.  In  either  case^  if  tlie  murmur  be  not 
transmitted  round  the  back,  the  first  sound  will  often  be 
heard  where  the  murmur  is  inaudible.      (Figs.  16  and  17.) 

Best  heard  at  the  apex-beat,  a  mitral  systolic  murmur 
may  be  conducted  with  diminishing  intensity  more  or 
less  widely  over  the  pra^cordia. 

The  murmur  may  be  transmitted  to  varying  extent, 
according  to  its  nature  and  causation,  through  the 
axillary  regions  to  the  angle  of  the  left  scapula. 


1 — r 


Fig.  16. — First  Sound,  Systolic  Muemur  ;  Double  Second,  Dias- 
tolic Murmur,  with  a  Sound-free  Interval  between  Double 
Second  Sound  and  the  Murmur. 

Significance. — Many  students  think  a  mitral  systolic 
murmur  indicates  mitral  stenosis,  but  it  only  means 
regurgitation  through  a  defective  valve.  It  means  this 
definitely;  but  the  actual  rhythm  of  the  murmur  gives 
no  information  as  to  the  condition  of  the  valve  which 
allows  of  leakage.  How  this  is  determined  must  now 
be  considered. 

Condition  of  the  mitral  valve  at  which  regurgitation 
takes  place. — In  investigating  the  condition  of  an  incom- 
petent mitral  valve  the  medical  history  of  the  patient  is 
of  the  greatest  importance.  Causes  of  cardiac  muscle 
failure  such  as  anaemia,  alcohol,  increased  arterial  ten- 
sion, diphtheria,  etc.,  likely  to  produce  mitral  dilatation, 
must  be  sought  for.     In  the  absence  of  such  a  cause  of 


74  HEART   DISEASE 

incompetence,  clinical  experience  and  pathological  find- 
ings have  shown  that  a  mitral  systolic  murmur  in  an 
adult  who  has  had  endocarditis  in  childhood  means 
regurgitation  through  a  stenosed  and  incompetent  valve 
in  the  great  majority  of  cases. 

Rheumatism  in  cliildliood. — The  indication  of 
endocarditis  in  childhood  is  a  history  of  acute  rheu- 
matism, chorea,  "  growing  pains,^'  or  scarlet  fever, 
and  careful  inquiry  will  show  that,  where  mitral 
stenosis  exists  in  adults,  nearly  every  one  of  the 
patients  will  give  such  a  history. 

Cases  do,  however^  occur  in  which  there  can  be 


1 — I — I — r 


Fig.  17. — Systolic  Muumur  avith  no  First  Sound,  accentuated 
Second  (kedui'licated  in  Second  Cycle), 

obtained  no  history  of  any  aches  or  pains  which 
generally  accompany  rheumatism  with  endocarditis, 
but  the  question  about  "growing  pains  "must  always 
be  put.  It  is  astonishing  how  often  an  adult  of 
fifty,  with  mitral  disease,  will  deny  having  had 
rheumatism  in  any  form,  but  will  remember  dis- 
tinctly severe  pains  as  a  child,  which  were  called 
"  growing  pains."  They  may  have  been  bad  enough 
to  interfere  with  school  or  work,  but  they  were  not 
called  rheumatic  either  by  the  doctor  or  by  the 
parents. 

It  must  be  remembered  that  in  infancy  the  ten- 
dency in  acute  rheumatism  is  for  the  joints  to  he  less 
involved,  for  there  to  he  less  pain  and  more  endocardial 


EHEUMATISM   IN   CHILDHOOD  75 

troiihle,  than  in  older  ages,  in  which  the  opposite 
conditions  tend  to  prevail.  There  may  even  be  no 
trivial  aches  or  pains,  and  the  sole  indication  of  an 
illness  in  which  the  slowly  progressing  valvulitis  is 
set  up  is  entirely  confined  to  the  heart,  with  the 
disease  so  insidious  and  slow  in  development  that 
even  breathlessness  and  debility  are  not  prominent. 
It  is  probable,  however,  that  in  nearly  all  these 
painless  endocarditis  cases  there  is  at  least  some 
debility,  if  it  only  be  recognized. 

A  severe  general  affection  of  the  heart,  endo- 
carditis, myocarditis  and  pericarditis  may  also  be 
set  up  and  lead  to  changes  which  can  not  be  made 
good,  and  which  cause  death  at  the  time  or  in  a 
few  years. 

Bheumatic  Nodules  are  sometimes,  but  not  com- 
monly, seen  in  children  suffering  from  acute  rheu- 
matism. They  are  almost  always  associated  with 
serious  heart  muscle  complications,  and  generally 
prognose  a  fatal  termination  before  long. 

The  ahseyice  of  a  ''rheiomatlc''  history  need  not  therefore 
exclude  the  diagnosis  of  mitral  stenosis  in  an  adult  in 
whom  the  regurgitation  is  found. 

The  reason  ivhy  the  diagnosis  of  mitral  stenosis  in  an 
adult  ivho  has  had  rheumatism  in  childhood  can  be  made 
is  that  the  simple  valvulitis  set  up  by  the  endocarditis 
then  is  a  very  slowly  progressing  disease  and  only 
causes  cardiac  symptoms  after  some  years,  whilst  the 
endocarditis  with  myocarditis  and  pericarditis  which  not 
uncommonly  complicates  rheumatism  in  childhood  and 
causes  dilatation  of  the  valve  orifice  through  severe 
muscle  failure  and  adherent  pericardium,  ends  fatally  at 
the  time  or  before  adult  life  is  reached. 


76  HEART   DISEASE 

Further  indications  of  the  condition  of  the  incom^ 
petent  mitral  valve. — Apart  from  the  above  evidence 
as  to  the  condition  of  the  valve  at  which  regurgitation 
is  taking  place,  clinical  experience  and  pathological 
findings  show  that  mitral  regurgitant  murmurs  which 
result  from  disease  of  the  valve  curtains  are  audible  more 
widely  than  those  which  result  from  cardiac  muscle  failure 
dilatation  of  the  valve  ring,  the  curtains  remaining  normal. 

This  is  probably  because  valve  vibration  murmurs  are 
transmitted  farther  than  those  of  fluid-vein  origin,  and 
are  heard  in  the  axilla  whilst  the  latter  are  not. 

If  an  incompetent  stenosed  valve  be  so  stiff  and  carti- 
laginous that  its  curtains  cannot  be  thrown  into  vibration 
by  a  regurgitant  stream  of  blood,  the  smooth  murmur  so 


T 

V5    '  VD   "^'     V5    '  VO 

Fig.  18. — Systolic  Murmuh,  Second  Sound  continued   by  Aortic 
Diastolic;  Systolic  and  Diastolic  Murmurs  with  no  Sounds. 

produced    will    not    be    propagated    towards  the   axilla 
farther  than  one  of  ordinary  fluid-vein  production. 

Cardiac  muscle  failure  regurgitant  murmurs j  as  has  been 
stated  before,  are  not  transmitted  into  the  axilla  like 
those  of  curtain  disease. 

The  prognosis  of  mitral  systolic  murmurs  depends 
entirely  on  the  condition  of  the  cardiac  muscle ;  the  less 
this  is  affected,  the  better  the  prognosis.  With  a  regular, 
slow  pulse  the  prognosis  may  be  quite  favourable;  it  is 
bad  with  a  quick,  irregular  pulse. 

As  it  has  been  said  on  a  previous  page,  a  loud  murmur 
does  not  necessarily  indicate  serious  disease  of  any  of 
the  cardiac  valves. 


MITRAL  MURMURS  77 

Mitral  diastolic  murmurs. — These  are  best  heard  at 
the  apex-beat,  and  are  not  transmitted  towards  the 
axilla.     They  may  be  heard  towards  the  tricuspid  region. 

Time. — They  almost  always  distinctly  follow  a  second 
sound,  which  is  frequently  reduplicated,  a  sound-free 
interval  occurring  between  the  sound  and  the  mnrmur' 
This  is  an  important  point  in  distinguishing  them  from 
aortic  diastolic  murmurs  with  which  often  no  second 
sound  is  heard,  or  which  follow  immediately  and  un- 
interruptedly on  a  second  sound,  if  one  be  present  (see 
Figs.  16  and  18). 

The  reason  why  mitral  diastolic  murmurs  generally 
follow  at  a  later  phase  of  v.d.  than  aortic  diastolic  mur- 
murs is  that  the  conditions  which  cause  them  are  later 
in  developing  than  with  the  aortic  murmur.  Thus  the 
main  forces  which  move  the  blood  from  auricle  to  ven- 
tricle^ namely,  active  ventricular  relaxation  or  diastole 
and  auricular  systole,  are  at  their  minimum  at  the 
beginning  of  ventricular  diastole,  whereas  those  driving 
blood  back  through  an  incompetent  aortic  valve  into  the 
ventricle  (elasticity  of  the  aorta)  are  at  their  maximum 
then. 

The  diastolic  murmur  varies  from  soft,  blowing,  to 
hard,  thrill-producing  characters,  and  is  decrescendo  in 
force. 

Cause. — Mitral  diastolic  murmurs  are  almost  invariably 
due  to  obstruction  at  the  stenosed  valve  to  the  flow  of 
blood  from  auricle  to  ventricle  during  diastole  of  the 
ventricle,  and  often  can  be  palpated  as  a  thrill. 

The  force  moving  the  blood  through  the  valve  is  that 
of  ventricular  aspiration  with  auricular  systole  helping 
at  the  end  of  ventricular  diastole  when  the  auricle  is 
strong  enough  to  contract. 


78  HEART   DISEASE 

A  diastolic  murmur  does  not  occur  in  every  case  of 
stenosis,  probably  because  the  contraction  of  the  auric- 
ular wall,  which  aids  in  its  production,  is  often  very 
feeble  or  entirely  absent  in  mitral  stenosis. 

A  few  cases  have  been  described  in  which  a  diastolic 
murmur  was  produced  at  a  dilated  mitral  valve.  An 
explanation  of  them  is  difficult  to  find. 

The  Prognosis  of  mitral  diastolic  murmurs  is  not 

good,  as  their  presence  indicates  some  definite  obstruction 
to  the  flow  of  blood  through  the  heart  which  may  lead 
to  auricular  muscle  failure  and  pulmonary  and,  finally 
systemic  venous  congestion. 


VD   ^     V3     ' 

Fig.  19. — Cuksoendo  Murmuh  (early  v.s.)  accentuated  First  Sound 
(delayed),  Accentuated  Second,  Pause,  Diastolic  Murmur. 

The  Mitral  crescendo  murmur  is  characterized  by 
rising  pitch,  increasing  force,  and  abrupt  termination 
with  accentuated  first  sound  at  its  highest  pitch  and 
maximum  force. 

It  has  been  argued  on  a  previous  page  that,  judging 
from  its  characteristic  of  rising  pitch,  this  murmur  must 
arise  at  an  orifice  which  closes  whilst  it  is  being  pro- 
duced. The  sound  oo-ij^,  produced  at  the  lips  only, 
demonstrates  this  point  clearly. 

The  mitral  valve  when  stenosed  is  often  so  diseased 
that  it  cannot  close  at  all  during  ventricular  systole, 
when  an  ordinary  systolic  murmur  of  uniform  pitch  and 
decrescendo  force  is  heard ;  or  it  can  only  be  closed 
at  a  later  phase  of  ventricular  systole  when  a  sufficient 


CRESCENDO  MURMUR  79 

amount  of  power  has  been  developed  to  force  together  the 
stiffened  rim  of  the  valve.  Whilst  this  force  is  gathering, 
blood  regurgitates  through  the  open  valve  and  produces 
a  systolic  murmur,  to  which  a  rising  pitch  character  is 
imparted  b}^  the  closing  of  the  valve. 

With  the  gathering*  force  which  closes  the  valve  the 
murmur  increases  in  vigour  or  becomes  crescendo  in  force. 

The  accentuated  first  sound  is  caused  by  forcible  co- 
aptation of  the  thickened  margins  of  the  valve,  and  has 
been  shown  to  arise  at  an  a])normally  late  phase  of  v.s. 

Time. — The  crescendo  murmur^  therefore^  is  early  v.s. 
or  presphygmic  in  rhythm,  and  occurs  immediately  before 
the  carotid  pulse. 


1 — r 

V5 


VD    ^S'     V5     I  VD 


Fig.  20.— Accentuated  Fiust  acjd  Doublk  Second  Sounds:  "wiih 
CiiESCENDO  Murmur  of  so-called  Pue-Systolic  Rhythm,  that 
IS,  Auricular  Systolic;  Systolic  Murmur;  Double  Second, 
Mitral  Diastolic  api'arently  continuous  with  following 
Pre-Systolic  Murmur. 


The  crescendo  murmur  varies  in  type  from  a  soft 
"  oo-ip "  sound  to  one  of  a  rougher  valve  vibration 
character. 

It  is  usually  taught  that  this  murmur  is  late  diastolic, 
auricular  systolic,  or  presystolic  in  rhythm  (Fig.  20), 
but  the  manner  of  its  causation,  in  my  opinion,  negatives 
this. 

Location. — Crescendo  murmurs  are  usually  only  heard 
at  the  apex  of  the  heart,  and  this  must  he  carefully  located 
and  the  stethoscope  applied  exactly  over  it.     They  are 


80  HEART    DISEASE 

rarely  transmitted  into  the  axilla,  possibly  because  the 
murmur  is  often  really  of  a  fluid-vein  type  and  lias  not 
wide  carrying  powers.  The  accentuated  first  sound  is 
generally  heard  in  the  axilla  and  at  the  back.  Occa- 
sionally, however,  a  crescendo  murmur  is  both  conducted 
towards  the  sternum  and  transmitted  into  the  axilla.  In 
these  cases  the  valve  probably  is  made  to  vibrate  by  the 
regurgitant  current  of  blood  which  causes  the  murmur. 

N.B. —  Whilst  a  crescendo  murTnivr  always  means  stenosis, 
the  absence  of  one  does  not  necessarily  mean  no  stenosis. 

The  Association  of  a  crescendo  murmur  with  other 
murmurs  in  mitral  stenosis  is  important. 

1.  It  may  be  the  only  murmui'  heard  in  mitral  stenosis. 

2.  It  may  follow  a  diastolic  murmur  (see  Figs.  19,  20 
and  21).  As  a  rule  there  is  a  sound-free  interval  be- 
tween the  decrescendo  diastolic  murmur  and  the 
crescendo  murmur.  Sometimes,  however,  there  is,  to 
the  ear,  no  interval  between  the  murmurs^  and  a  con- 
tinuous murmur  apparently  runs  from  after  the  second 
sound  to  the  accentuated  first  sound.  This  is  one  reason 
advanced  in  support  of  the  auricular  systolic  or  pre- 
systolic rhythm  theory  of  the  murmur,  for  it  is  said  that 
such  an  apparently  continuous  sound  must  be  produced 
by  blood  flowing  in  the  same  direction  through  the 
valve.  This  argument  can  be  used  to  prove  that  it  is 
early  systolic  in  rhythm  (see  paragraph  3  below). 

When  the  diastolic  murmur  is  apparently  continuous 
with  the  crescendo  murmur,  it  probably  means  that  the 
auricle  is  able  to  contract  in  its  proper  rhythm — namely, 
just  before  v.s.,  and  so  keep  u])  the  true  diastolic 
murmur. 

Very  often  in  mitral  stenosis  the  auricle  is  so  dilated 
and  weakened  as  to  he  unable  to  contract  ivith  sufficient 


CRESCENDO  MURMUR  81 

force  to  help  in  cmt-nng  a  diastolic  murmur.  I  believe 
that  this  explains  the  frequent  absence  of  this  murmur 
in  mitral  stenosis. 

3.  A  crescendo  murmur  may  he  uninterruptedly  folloiced 
by  a  systolic  murmivr.  This  occurs  when  the  curtains  are 
so  distorted  by  disease  that,  although  their  edges  are 
brought  into  apposition  abnormally  late  in  ventricular 
systole  (crescendo  murmur),  they  still  are  unable  to  com- 
pletely close  the  orifice,  and  a  leak  is  left  through  which 
blood  continues  to  regurgitate  throughout  ventricular 
systole  and  continues  the  crescendo  murmur  as  a  systolic 
murmur  (see  Fig.  14,  E  and  F).  These  two  murmurs 
are  produced  at  the  mitral  valve  by  the  continuous  action 


J 


T— -I p-r \ \ ; 1 r— ! p-i — ^ 1 r—, r*— , . 

Fig.  21. — CRESCExno  Murmur  (early  v.s.  Rhythm),  Double  Second 
Mitral  Diastolic,  Sound-free  Interval,  then"  Crescendo 
Murmur  again,  followed  by  Systolic  Murmur,  etc. 

The  first  is  the  commoner  condition,  the  continuous  diastolic  and  cres- 
cendo murmur,  depicted  in  the  second  cycle,  being  not  so  common. 

of  the  ventricle  in  its  successive  stages  of  systole,  and 
are  continuous,  though  so  very  dissimilar  in  character. 
The  impact  of  those  portions  of  the  thickened  valve 
curtains  which  can  come  into  apposition  causes  the 
accentuated  first  sound  which  delimits  these  murmurs. 

4.  A  systolic  murmur  may  change  into  a  crescendo 
murmur  within  a  few  heart-beats  and  vice  tersa.  When 
the  ventricle  is  not  contracting  with  sufficient  force 
to  close  the  valve,  a  systolic  murmur  of  regurgitation 
is  heard.  If  the  force  of  contraction  be  increased,  as  by 
making  the  patient  sit  up  in  bed,  the  valve  is  then 
closed  and  the  crescendo  murmur  developed.     When  the 

6 


82  HEART   DISEASE 

patient  lies  down  and  the  extra  force  of  ventricular 
systole  is  reduced,  the  systolic  murmur  again  appears. 
To  put  it  in  another  way,  a  systolic  murmur  may  be 
heard  when  the  patient  is  up  and  about  and  overworking 
the  heart,  Avhich  is  replaced  by  a  crescendo  murmur 
after  rest  in  bed  and  treatment  by  digitalis. 

5.  Crescendo,  systolic,  and  diastolic  murmurs  may  all  he 
heard  during  one  cardiac  cycle,  with  accentuated  first 
and  double  second  sounds  (see  Fig.  21). 

Prognosis  of  crescendo  murmurs, — The  presence  of  a 
crescendo  murmur  means  that  the  ventricle  is  contract- 
ing well  and  that  regurgitation  through  the  valve  is 
reduced  to  a  minimum,  and  less  than  when  a  systolic 
murmur  is  heard.  I  look  upon  it  as  a  favourable  sign, 
for  it  often  is  only  heard  after  overworked  heart  muscle 
recovers  its  tone  through  rest  in  bed  and  treatment. 

Tricuspid  Muemuks. 

Lesions  of  the  tricuspid  valve  are  much  less  common 
than  those  of  its  fellow  valve,  and  are  often  difficult  to 
diagnose.  They  are,  however^  often  accompanied  by 
evidence  of  back-pressure  in  the  pulmonary  arterial 
or  systemic  venous  circulations,  and  this  evidence  is 
useful. 

Tricuspid  systolic  murmurs  are  best  heard  over  the 
heart  between  the  apex  and  the  tricuspid  region.  They 
are  similar  to  mitral  murmurs  in  origin  and  charac- 
teristics, but  are  not  transmitted  through  the  axillary 
region.  They  are  often  hard  to  differentiate  from 
mitral  murmurs,  and  often  heard  with  them. 

When  a  systolic  murmur  is  heard  to  the  right  of  the 
sternum,  and  there  is  evidence  of    enlargement  of  the 


TRICUSPID  AND  AORTIC  MURMURS  83 

right  auricle  and  pulmonary  and  general  venous  conges- 
tion, it  is  almost  certainly  due  to  tricuspid  incompe- 
tence. 

Tricuspid  diastolic  murmurs  are  similar  in  char- 
acteristics to  mitral  murmurs,  but  may  be  conducted 
slightly  to  the  right  of  the  sternum,  especially  with 
dilatation  of  the  right  auricle.     They  are  not  common. 

The  tricuspid  crescendo  murmur  is  of  similar  origin 
and  characteristics  to  the  mitral  murmur  of  the  same 
name. 

With  both  diastolic  and  crescendo  murmurs  there 
would  be  evidence  of  systemic  venous  congestion, 
enlargement  of  the  liver  and  general  oedema,  and  also 
of  pulmonary  circulation  congestion. 

The  prognosis  of  tricuspid  murmurs  is  not  good,  as 
disease  of  this  valve  impedes  the  return  of  venous  blood 
to  the  lungs  and  induces  general  oedema  and  secondary 
cardiac  muscle  failure. 

Aortic  Murmurs. 

Lesions  of  the  aortic  valve  are  not  so  common  as  those 
of  the  mitral  valve. 

Aortic  systolic  murmurs  vary  in  nature  according  to 
their  causes.  In  relative  stenosis,  due  to  dilatation  of 
the  aorta,  they  ought  to  be  of  the  softer  fluid-vein  type ; 
but,  as  a  matter  of  fact,  when  relative  stenosis  occurs  at 
this  valve,  there  is  generally  some  atheroma  of  the  aorta 
as  well  which  affects  the  curtains  of  the  valve  also, 
roughening  and  stiffening  them  more  or  less,  and  giving 
rise  to  the  rougher,  more  intense  vibration  murmur  of 
actual  stenosis.     Sometimes  they  are  of  a  musical  char- 


84  HEART   DISEASE 

acter,  in  which  case  a  tag  of  fibrin  may  be  vibrated  by 
the  blood- stream.  When  actual  stenosis  exists,  or  Avhen 
the  curtains  are  much  changed,  a  thrill  can  often  be  felt 
over  or  above  the  aortic  area. 

They  are  best  heard  in  the  aortic  area,  whence  they 
are  conducted  into  the  great  arteries,  and  are  especially 
well  heard  over  the  carotids  without  any  pressure  from 
the  stethoscope. 

They  may  be  heard  down  the  cardiac  area  to  the  apex- 
beat,  gradually  diminishing  in  intensity  all  the  way.  It 
is  therefore  important  to  listen  to  an  apex  murmur  over 
different  portions  of  the  pra^cordia  between  the  apex  and 
the  aortic  area.  A  murmur  which  grows  in  intensity 
when  followed  in  this  way  indicates  an  aortic  (or 
pulmonary)  murmur,  and  one  which  diminishes  a  mitral 
(or  tricuspid)  murmur. 

Aortic  sj'Stolic  murmurs  are  of  a  decrescendo  nature, 
fading  away  with  cessation  of  v.s. 

If  an  aortic  systolic  murmur  be  due  to  actual  stenosis, 
the  radial  pulse  is  regularly  delayed. 

Time. — Aortic  systolic  murmurs  are  synchronous  with 
the  carotid  pulse,  and  should  always  be  timed  by  it, 
because  a  loud  diastolic  murmur  may  alone  be  present 
and  simulate  one. 

Aortic  diastolic  murmurs  vary  in  intensity  from  a 
loud,  rough,  easily  audible  sound  to  the  faintest  whiif, 
which  is  the  most  difficult  of  all  cardiac  murmurs  to 
recognize.  The  difficulty  of  hearing  the  short  faint  aortic 
diastolic  murmurs  is  increased  by  the  fact  that  they 
may  be  audible  only  at  the  tricuspid  region  of  the  heart, 
and  they  are  very  commonly  overlooked.  Their  presence 
may  be  suspected  by  the  change  in  the  second  sound 
when   they  are  associated   with  one.     The  sound  is  no 


AORTIC  MURMURS  85 

longer  distinct  and  clear;  it  is  impure,  and  apparently 
prolonged  into  a  whiff  or  faint  blow,  as  if  the  ^'  bottom 
were  knocked  out "  of  the  sound  (see  Fig.  18). 

An  aortic  diastolic  murmur  is  particularly  difficult  to 
hear  if  there  be  a  co-existent  mitral  diastolic  murmur. 

This  short  diastolic  murmur  may  be  cau.^ed  by  a  similar 
mechanism  to  that  which  produces  an  a.-v.  crescendo 
murmur,  and  have  some  of  the  rising  pitch  character- 
istic of  this  murmur  (p.  59).  The  short  duration  of  it 
can  hardly  be  due  to  inability  of  the  contracting  aorta 
to  keep  up  the  murmur,  for  aortic  diastolic  murmurs 
are  generally  more  prolonged. 

The  important  difference  in  rhythm  hetiveen  aortic  and 
mitral  diastolic  murmurs — namely,  that  the  latter  begin 
at  a  later  phase  of  ventricular  diastole  than  the  former — 
has  already  been  pointed  out,  and  reasons  why  such 
should  be  so  given  (see  Figs.  16  and  18). 

Condition  of  ttie  aortic  valve  at  wliicli  regurgitation 
occurs, — The  diastolic  murmur  may  continue  a  distinct 
aortic  second  sound,  in  which  case  the  curtains  are  mobile 
and  more  or  less  normal,  perhaps  with  dilatation  of  the 
valve  ring ;  or  there  may  be  no  aortic  second  sound,  in 
which  case  the  leakage  results  from  a  stenosed  valve  with 
thickened,  rigid,  immovable  curtains.  The  latter  form 
of  murmur  is  rougher  than  the  former. 

Sometimes  the  aortic  diastolic  murmur  is  the  only 
murmur  present,  and,  unless  it  be  timed  by  the  carotid 
artery,  will  very  likely  be  mistaken  for  a  systolic  murmur, 
especially  by  the  student,  who  is  inclined  to  look  upon 
all  murmurs  as  systolic  unless  they  prove  themselves  to 
be  diastolic. 

Like  all  other  murmurs,  except  the  crescendo  murmur, 
they  are  of  diminishing  intensity,  or  decrescendo. 


S6  HEART  DISEASE 

Crescendo  aortic  murmurs. — The  possibility  of  an 
aortic  diastolic  murmur  having  some  rising  pitch  char- 
acter has  already  been  referred  to  above  and  in  the 
paragraph  on  crescendo  murmurs  (p.  85). 

See=saw  or  *'  To=and-fro"  murmur, — Not  uncom- 
monly the  aortic  diastolic  murmur  follows  immediately  an 
aortic  systolic  murmur^  giving  a  to-and-fro  characteristic 
known  as  the  "  see-saw  murmur."  If  the  lesion  be  one 
of  absolute  stenosis  with  incompetence,  an  aortic  second 


Fig.   22.— See-Saw  Aoktic  Mukmuk,  continuous,   no  Sounj>s,  but 
THE  Diastolic  I'oiiTioN  akises  immediately  at  the  End  of  v.s., 

AND  not  after  A  SoUND-FllEE  InTEUVAL,  AS  IN  MlTllAL  DIASTOLIC 

MuiiMuns. 

sound  is  rarely  heard.  If  it  be  one  of  relative  stenosis 
with  aortic  dilatation  or  aneurysm,  a  sound  may  in- 
tervene. 

Prognosis  of  aortic  murmurs. — Aortic  systolic  mur- 
murs  generally  indicate  actual  obstruction  to  the  flow  of 
blood  from,  and  increase  in  the  work  done  by,  the  left 
ventricle.  Sliglit  obstruction  may  be  easily  compensated 
by  ventricular  hypertrophy,  and  if  this  is  adequate  the 
condition  may  not  affect  the  duration  of  life.  When 
greater,  the  ventricle  may  be  unable  to  respond  ade- 
quately; it  fails  or  dilates,  and  the  outlook  is  bad. 

When  aortic  systolic  murmurs  indicate  relative  obstruc- 
tion of  the  orifice  with  a  dilated  aorta  or  an  aneurysm 
beyond,  the  prognosis  is  serious. 

Aortic  diastolic  m?tr//iwr.9,  indicating  incompetence  of  the 
valve,  are  more  serious.     Slight  degrees  of  regurgitation 


POSTURE  MURMUR  87 

may  be  adequately  counteracted  by  efficient  ventricular 
hypertrophy,  and  may  be  present  for  years  without 
adversely  affecting  the  health.  When  the  leakage  is 
greater  the  strain  on  the  left  ventricle  is  very  great,  and 
adequate  compensation  becomes  impossible.  The  out- 
look is  then  most  serious,  sudden  overstrain  of  the  heart 
with  fatal  syncope  being  a  common  ending. 

The  condition  of  the  muscle  of  the  left  ventricle  is  the 
determining  factor  in  prognosis  of  both  forms  of  aortic 
disease,  as  it  is  in  all  other  forms  of  valvular  disease. 

Posture  murmur. — A  very  well-marked  systolic  mur- 
mur, simulating  exactly  an  aortic  murmur,  is  sometimes 
heard  over  the  manubrium  sterni  and  base  of  the  heart 
in  quite  healthy  persons  who  are  holding  the  shoulders 
well  back,  and  probably  thereby  causing  some  pressure 
of  the  collar-bone  on  the  subclavian  artery.  Such  a 
murmur  may  be  heard  when  the  subject  being  examined 
is  holding  his  vest  well  up  for  auscultation  at  the  base 
of  the  heart.  It  disappears  at  once  if  the  shoulders  are 
brought  forward  to  remove  the  pressure.  The  murmur 
is  so  deceptive  that  it  may  create  the  impression  of  some 
aortic  valve  disease.     (See  also  p.  67.) 

Pulmonary  Murmurs. 

Pulmonary  murmurs  are  very  much  like  those  pro- 
duced at  the  aortic  valve  in  nature.  Structural  changes 
in  the  valves  do  not  often  arise  in  adult  life,  and  when 
met  with  then  are  almost  always  congenital  in  origin. 

Pulmonary  systolic  murmur. — This  is  not  uncom- 
monly heard  in  marked  anaemia,  when  it  is  caused  by 
relative  stenosis  of  the  valve  orifice,  the  pulmonary  artery 
beyond  the  valve  frequently  dilating,  for  some  reason  or 
other  not  understood,  in  anemic  conditions  of  the  blood. 


88  HEART  DISEASE 

It  may  be  met  with  in  apparently  healthy  persons,  and 
may  mean  nothing ;  and  it  is  also  commonly  heard  in 
mitral  stenosis.    It  is  frequently  heard  in  Graves'  disease. 

A  systolic  murmur  due  to  structural  changes  of  the 
curtains  is  by  no  means  common  in  adult  life,  but  is 
more  often  heard  in  childhood. 

Actual  stenosis  of  the  valve  occurs  as  a  congenital 
deformity,  but  generally  causes  death  before  adult  life. 
It  may  be  present  in  young  adults,  when  cyanosis  will  be 
a  marked  feature  of  the  circulation. 

Conduction, — Pulmonary  systolic  murmurs  are  not 
conducted  into  the  carotid  or  subclavian  arteries,  but  are 
conducted  or  transmitted  over  the  left  second  intercostal 
space  well  away  from  the  sternum. 

Pulmonary  diastolic  murmurs  are  very  rare,  but 
when  heard  have  much  the  same  area  of  conduction, 
down  the  left  margin  of  the  sternum,  as  the  analogous 
aortic  murmur,  with,  however,  the  pulmonary  cartilage 
as  the  theoretical  seat  of  maximum  intensity. 

Prognosis. 

Prognosis  in  pulmonary  murmurs. — If  due  to  anaemia 
the  prognosis  is  that  of  the  primary  cause.  If  due  to 
structural  changes  it  is  bad,  and  subjects  of  pulmonary 
valve  disease  rarely  reach  adult  life. 


VIII 
HiEMIC  MURMURS 

Cardiac  haemic  murmurs,  which  are  of  a  soft,  blow- 
ing character,  are  met  with  in  anaemic  conditions  of  the 
blood,  and  without  there  being  any  disease  of  the  valve 
curtains.  They  are  systolic  in  rhythm,  and  not  con- 
ducted widely.  Their  causation  has  been  much  debated. 
It  is  very  doubtful,  as  has  already  been  stated,  whether 
the  diminished  viscosity  of  the  blood  itself  has  anything 
to  do  with  the  production  of  the  murmur.  Moreover,  it  is 
important  to  remember  that  in  chlorosis,  in  which  these 
murmurs  commonly  occur,  there  is  sometimes  tivo  or 
three  times  the  normal  volume  of  blood  present,  and  this 
may  lead  to  abnormal  distension  of  cavities  and  so  to  the 
easier  production  of  fluid-veins,  especially  at  the  semi- 
lunar valve  orifices. 

The  commonest  situation  for  them  to  be  heard  is  at 
the  base  of  the  heart  over  the  pulmonary  cartilage  and 
in  the  second  left  intercostal  space.  The  murmur  thus 
heard  is  probably  due  to  there  being  relative  stenosis  of 
the  pulmonary  valve,  experience  having  shown  that  this 
artery  immediately  beyond  its  valve  is  often  dilated  in 
marked  angemia. 

A  haemic  murmur  may  also  be  heard  over  the  apex 
in  severe  anemia.  In  these  cases  there  is  generally  some 
dilatation  of  the  ventricle,  and  the  murmur  is  one  of 
valvular  incompetence  arising  from  muscle  failure. 

89 


90  HEART  DISEASE 

They  are  often  heard  best  with  the  quicker  hearths 
action  of  the  erect  position,  and  disappear  when  the 
patient  lies  down,  or  the  heart's  action  slows. 

Vascular  haemic  murmurs  are  heard  over  the  large 
vessels  with  or  without  slight  pressure  from  the  stetho- 
scope. If  pressure  is  used  the  constriction  of  the 
vessel  produces  a  fluid  vein. 

Bruit  de  diable- — This  is  best  heard  over  the  veins 
about  the  attachment  of  the  sterno-mastoid  to  the 
sternum,  and  without  any  pressure  from  the  stethoscope. 
It  is  of  a  continuous  humming  or  buzzing  character  and 
is  probably  only  heard  in  chlorosis  where  we  have  an 
increased  volume  of  blood,  sometimes  more  than  double 
the  normal  amount,  in  addition  to  diminished  viscosit^^ 
It  is  possible  that  the  continuity  of  the  hum  is  due  to  the 
abnormal  distension  of  the  large  veins  in  this  disease 
forming  large  masses  of  blood  into  which  comparatively 
small  streams  pass  from  the  tributary  veins  with  an 
abnormal  head  of  pressure  produced  in  the  overfull 
capillaries.  Diminished  viscosity  may  also  contribute 
in  some  unknown  way  to  its  production. 

The  hum  can  also  be  heard  by  placing  the  stethoscope 
lightly  over  the  ball  of  the  eye,  the  mastoid  region,  or 
on  the  occiput  over  the  site  of  the  torcular  Herophili. 
In  these  situations  the  stethoscope  is  close  to  the  cavern- 
ous sinuses  of  the  skull. 

The  hridt  de  diahle  is  rarely  met  with  in  severe  anaemia 
without  increased  volume  of  blood ;  in  these  cases,  in- 
stead of  a  continuous  hum,  the  murmur  over  the  veins  is 
of  a  broken,  swishing,  rhythmic  nature. 

Like  true  chlorosis,  it  is  uncommon  in  Manchester. 


IX 
EXOCARDIAL   SOUNDS 

These  sounds  are  produced  outside  the  cavities  of  the 
heart. 

Pericardial  sounds. — Normally  the  smooth  surfaces 
of  the  visceral  and  parietal  layers  of  the  pericardium 
move  over  each  other  without  any  audible  sound^  but 
when  this  membrane  is  inflamed,  as  it  is  in  pericarditis, 
and  becomes  rough,  then  the  movement  of  the  two 
roughened  surfaces  against  each  other  causes  a  sound 
known  as  a  pericardial  rub  or  friction  sound. 

This  pericardial  rub  varies  greatly  in  character  from  a 
very  slight,  almost  inaudible  sound  to  a  marked,  rough, 
leathery  creaking,  the  latter  being  occasionally  so  well 
developed  as  to  be  palpable  to  the  hand. 

The  pericardial  rub  frequently  simulates  an  endocardial 
sound,  but  usually  is  easily  differentiated  from  it. 

It  is  generally  a  double  or  to-and-fro  sound,  corre- 
sponding roughly  with  systole  and  diastole  of  the  heart, 
and  is  well  imitated  by  rubbing  the  balls  of  the  thumbs 
over  each  other  and  in  a  to-and-fro  movement  with  vary- 
ing degrees  of  pressure. 

In  some  instances  one  or  other  parts  of  the  sound  may 
be  double,  imparting  to  it  a  shuffling  character. 

Pericardial  friction  is  generally  best  heard  over  the 
base  of  the  heart,  and  often  can  be  intensified  by  gentle 

91 


92  HEART   DISEASE 

pressure  u-ith  the  stethoscope,  wliich  has  for  its  object  the 
bringing  of  the  two  layers  of  the  pericardium  more 
closely  together.  It  is  unchanged  by  holding  the 
breath,  and  may  only  be  heard  for  a  day  or  so. 

When  fluid  develops  and,  by  distending  the  pericardial 
sac,  separates  the  two  sufaces  the  rub  will  disappear, 
possibly  to  reappear  with  the  absorption  of  the  fluid. 

The  sound  is  not  conducted  away  from  its  seat  of 
origin  unless  it  be  very  loud,  in  which  case  it  may  be 
transmitted  slightly  beyond  the  limits  of  the  pr^cordia. 

Cardio-Pespiratory  sounds. — Occasionally  sounds  are 
produced  by  the  movements  of  the  heart  acting  on  the 
lungs  or  pleura  which  may  simulate  endocardial  or 
pericardial  sounds  ;  but  they  are,  as  a  rule,  easily 
differentiated  from  the  endocardial  sounds  because  they 
vary  with  the  respiratory  movements,  and  because 
the  sounds  of  the  heart  are  heard  as  usual. 

Card io= pulmonary  sounds. — Respiratory  sounds  syn- 
chronous with  systole  of  the  ventricle  may  be  heard 
when  an  emphysematous  lung  comes  forward  over  the 
heart  and  is  compressed  by  the  movements  of  the  heart. 

Such  a  sound  may  simulate  an  endocardial  murmur, 
but  it  is  loudest  with  expiration  and  disappears  when 
the  breath  is  held  on  full  inspiration.  It  may  also 
resemble  the  creaking  of  a  saddle. 

CardiO'pleural  sounds. — With  inflammation  of  the 
pleura  over  the  front  of  a  lung  a  sound  of  friction  may 
be  caused  by  the  movements  of  the  heart  pressing  the 
two  pleural  surfaces  together.  Such  a  sound  may  closely 
simulate  a  pericardial  rub  and  will  not  vary  with  inspira- 
tion . 


SEPTIC   ENDOCARDITIS, 
PERICARDITIS,  ANGINA  PECTORIS 

Septic,  maligrnant,   op  ulcerative   Endocarditis  is 

not  uncommonly  met  with,  especially  in  the  practice  of  a 
general  hospital.  It  is  also,  unfortunately,  not  uncom- 
monly unrecognized  during  life,  as  an  elevated  tempera- 
ture, often  in  the  form  of  rigors,  and  evidence  of  great 
debility  are  the  only  physical  signs  present.  The  heart 
sounds  may  be  quite  free  from  murmur. 

In  typical  cases  with  elevated  temperature,  murmurs, 
enlarged  spleen,  hematuria  and  infarcts  the  diagnosis  is 
straightforward . 

Its  presence  must  always  be  suspected  when  there  is 
prolonged  elevation  of  temperature  in  cases  of  chronic 
valvular  disease. 

Treatment  is  very  unsatisfactory.  In  some  of  the 
cases  complicating  chronic  endocarditis  the  acuteness 
subsides  and  the  chronic  condition  remains  much  as 
before,  but  the  acute  cases  arising  de  novo  almost  in- 
variably end  fatally.  Vaccine  treatment  by  autogenous 
vaccines  where  the  organism  can  be  isolated,  which  is, 
however,  very  difficult  to  do,  is  reported  to  have  relieved 
a  few  cases,  but  all  treatment  is  as  a  rule  unavailing. 

93 


94  HEART   DISEASE 

Pericapditis  generally  occurs  as  a  complication  of 
rheumatic  infection,  but  may  be  found  in  gout,  cachectic 
conditions  and  (N.B.)  acute  pneumonia. 

Simple  acute  pericarditis  results  in  the  exudation  of 
lymph  which  in  the  most  favourable  cases  is  soon  re- 
absorbed without  any  permanent  damage.  Its  presence 
is  recognized  by  the  associated  endocarditis,  by  some 
respiratory  distress,  and  by  pericardial  friction  {q.v.), 
which  may  be  heard  with  the  stethoscope.  Pain  is  not 
a  prominent  symptom,  and  for  this  reason  pericarditis 
is  often  overlooked.  In  less  favourable  cases  the 
inflammation  may  become  dry  and  persist  for  a  longer 
time,  clearing  up  eventually  or  leading  to  the  formation 
of  adhesions  and  adherent  pericardium.  Dry  pericarditis 
may  be  felt  by  the  hand,  causing  a  rubbing  sensation  be- 
hind the  praecordia,  and  it  can  be  heard  by  the  stethoscope. 

The  danger  to  the  patient  in  most  cases  is  not  the 
actual  pericardial  inflammation  itself,  but  the  fact  that 
it  is  evidence  of  an  acute  inflammation  of  the  whole  of 
the  cardiac  tissue — endo-,  myo-,  and  pericardium.  A 
patient  with  acute  pericarditis  is  always  in  danger,  the 
termination  being  not  infrequently  remarkably  sudden. 

Pericardial  effusion. — The  inflammation  of  the  peri- 
cardium may  lead  to  effusion  of  serous  fluid  in  greater 
or  less  amount.  Fluid  may  be  suspected  if  a  rub  passes 
off  in  a  day  or  so  and  reappears  in  a  few  days.  If  it  is 
poured  out  in  large  quantity  it  causes  increased  cardiac 
dulness,  especially  in  an  upward  direction^  by  distending 
the  sac  into  a  pear-shaped  body  which  can  be  made  out 
by  percussion,  the  broad  part  being  about  the  line  of  the 
fourth  intercostal  space.  The  intercostal  spaces  of  the 
pra3Cordia  may  be  distended.  The  impulse  of  the  apex- 
beat  diminishes  in  intensity  and  is  internal  to  the  limits 


ADHERENT  PERICARDIUM  95 

of  cardiac  dulness.  The  heart  sounds  are  muffled  or 
weakened,  and  the  apex  may  be  pushed  up  and  out. 
There  is  a  good  deal  of  respiratory  distress,  due  to  the 
interference  with  the  hearths  action,  which  makes  the 
sitting-up  (orthopnoea)  position  necessary.  The  pulse  is 
also  quick,  120  or  more,  and  there  is  much  pallor. 
Serous  effusions  tend  to  be  absorbed  in  time,  and  opera- 
tive interference — paracentesis  pericardii — is  not  often 
advisable. 

Purulent  pericarditis  is  often  only  recognized  post 
mortem,  and  its  diagnosis  in  life  is  quite  uncertain. 

Adherent  pericardium  is  most  likely  to  be  met  with 
before  adolescence,  but  it  is  more  often  found  in  the 
post-mortem  room  than  diagnosed  in  the  wards.  Patients 
in  whom  it  is  present  rarely  reach  adult  life.  It  may  be 
suspected  when  severe  rheumatic  inflammation  of  the 
endocardium,  myocardium,  and  pericardium  has  led  to 
considerable  dilatation  of  the  heart  which  persists  per- 
manently after  subsidence  of  the  acute  symptoms,  and 
in  spite  of  treatment  by  prolonged  rest  in  bed  and 
especially  by  digitalis.  Uncomplicated  dilatation  of  the 
ventricles  often  recovers  very  well  after  such  treatment, 
but  if  the  inflamed  pericardium  covering  the  enlarged 
ventricles  adheres  to  the  inflamed  outer  layer  of  the 
pericardial  sac  subsequent  shrinking  of  the  muscle 
becomes  impossible. 

In  adherent  pericardium  there  may  be  systolic  retrac- 
tion of  the  intercostal  spaces  between  the  left  lateral 
sternal  line  and  the  region  of  the  apex  of  the  enlarged 
heart,  with  synchronous  protrusion  of  the  apex  of  the 
heart.  Such  a  condition,  however,  may  be  met  with 
when  there  is  considerable  cardiac  enlargement  with  no 
pericardial  adhesion,    the   systole    of   the    base    of   the 


96  HEART   DISEASE 

enlarged  right  ventricle  causing  negative  pressure  in  the 
chest  which  leads  to  retraction  of  the  intercostal  spaces 
in  front  of  it.  When  the  heart  is  much  enlarged  and 
the  two  layers  of  the  pericardium  are  coherent  con- 
traction of  the  heart  may  pull  on  the  diaphragm^  and 
consequently  on  its  attachments  to  the  ribs  in  the  axillary 
and  posterior  regions  of  the  chest_,  causing  systolic  in- 
drawing  of  the  regions  of  the  diaphragmatic  attachment. 

On  auscultation  a  systolic  murmur,  indicating  incom- 
petence through  dilatation  of  the  mitral  valve,  will 
generally  be  heard. 

There  are  also  present  signs  of  interference  with  the 
action  of  the  heart  muscle  leading  to  back  pressure  in 
the  pulmonary  and  systemic  circulations. 

Pericardial  adhesion  may  be  a  part  of  a  process  leading 
to  a  general  mediastinal  inflammation  which  has  a 
special  group  of  symptoms,  or  of  a  process  leading  to 
inflammation  of  all  the  serous  membranes  of  the  trunk, 
— the  pericardium,  pleura  and  peritoneum. 

Angfina  pectOPis  is  the  term  given  to  the  extremely 
distressing  and  painful  condition  which  results  from 
interference  with  the  circulation  of  blood  through  the 
heart  muscle  itself  by  some  obstruction  of  the  coronary 
arteries  or  by  overworking  a  heart  with  enfeebled 
muscle.  The  pain  is  of  two  kinds — a  heavy,  suffocating 
feeling  behind  the  sternum  or  of  something  gripping 
the  heart  and  giving  rise  to  a  sensation  of  impending 
death;  and  shooting  neuralgic  pains  down  the  arm, 
especially  the  left  arm,  to  the  elbow  or  even  to  the  little 
and  ring  fingers,  up  the  neck  behind  the  ear,  and  into 
the  left  shoulder-joint. 

Diagnosis, — Angina  pectoris  may  occur  without  there 
being  the  slightest  auscultatory  evidence  of  any  cardiac 


ANGINA  PECTORIS  9? 

disease ;  when  there  is  evidence  of  aortic  disease, 
atheroma,  or  aneurysm  ;  of  mitral  stenosis  or  of  severe 
cardiac  muscle  failure  or  debility.  It  is  not  uncommonly 
fatal  in  its  first  appearance,  but  more  often  it  recurs  at 
intervals  over  longer  or  shorter  periods  of  time.  It  is 
generally  made  worse  by  exertion,  but  it  may  be  brought 
on  through  the  interference  with  the  hearths  action 
which  a  stomach  distended  with  flatulence  often  gives 
rise  to. 


XI 


CARDIAC    IRREGULARITY 

RESULTING  FROM  DISTURBANCES 

OF    STIMULATION 

Electrocardiogram. — The  different  phases  of  the 
cardiac  cycle  can  be  timed  with  great  accuracy  by  means 
of  the  property  which  muscle  has  of  giving  rise  to 
currents  of  electricity  by  its  contraction.  These  currents 
are  very  slight,  and  they  need  the  most  delicate  instru- 
ments for  receiving  and  recording  them.  The  instrument 
now  used,  the  string-galvanometer,  is  an  elaboration  and 
improvement  of  that  originally  used  as  a  receiver  in  the 
first  days  of  transatlantic  telegraphy.  The  principle  of 
it  is  that  the  minute  current  of  electricity  generated  by 
the  muscle  contraction  is  carried  on  a  silvered  filament 
of  rock  crystal  or  on  some  suitable  wire  between  the 
live  poles  of  a  strong  electro-magnet  and  according  to 
whether  the  current  passing  is  +  or  —  so  will  the  string- 
be  deflected  to  the  —  or  +  pole.  The  movements  of  the 
string  are  recorded  by  the  shadow  which  is  cast  by  it, 
on  a  moving  sensitized  roll  of  photographic  paper  between 
which  and  a  light  it  also  lies.  The  tracing  is  very  small, 
and  has  to  be  magnified  subsequently  to  get  the  record 
which  is  to  be  used  for  observation. 

With  a  normal   heart  contracting,  a  regular  type  of 

98 


RAPID   HEART-BEAT  99 

electrocardiogram  is  obtained  showing  movements  which 
are  caused  by  the  currents  induced  by  contraction  and 
relaxation  of  the  auricles  and  ventricles.  Departures 
from  the  normal  rate,  rhythm  and  method  of  contraction 
of  the  auricles  or  ventricles  show  corresponding  depar- 
tures from  the  normal  cardiographic  tracing. 

An  electrocardiogram  is  generally  taken  synchronously 
with  one  or  more  other  tracings  taken  from  the  carotid 
or  radial  artery  or  the  jugular  vein ;  a  phonoscope  re- 
cording the  sounds  produced  in  the  heart  may  be  used 
at  the  same  time  as  well.  The  most  elaborate  tracings 
give  all  of  these  synchronously  with  a  time  record  also. 

The  electrocardiograph  is  a  very  valuable  instrument 
for  the  investigation  of  cardiac  disease,  but  its  cost 
(£200)  and  the  laboratory  accommodation  necessary  for 
its  use  practically  restricts  its  employment  to  hospitals. 

Tachycardia  means  quick  hearths  action,  over  130  a 
minute,  but  its  use  as  a  term  is  best  restricted  to  a  more 
rapid  action  which  is  the  result  of  some  patholoD*ical 
change  in  the  hearths  nervous  mechanism  or  musculature. 

The  apprehensive  heart.— A  very  rapid  beat  is  often 
met  with  in  a  heart  unaffected  by  disease  when  the 
patient  is  of  a  nervous,  apprehensive  type.  The  so-called 
insurance  heart  and  the  legal  neurasthenic  heart  are 
of  this  nature.  I  have  counted  a  pulse  of  above  160  in 
a  girl  who  was  being  treated  with  zinc  ionization  for 
oesophageal  ulcer.  The  heart  was  structurally  normal 
and  slowed  down  to  its  proper  rate  within  a  couple  of 
hours  after  the  exciting  experience.  A  rate  of  130  is 
not  uncommon  in  insurance  work.  In  this  type  of  rapid 
heart  action  the  quickness  varies  even  within  a  few^ 
seconds.  The  heart  may  slow  down  almost  to  normal 
after  a  time,  or  when  the  subject  lies  down,  only  to  race 


100  HEART   DISEASE 

off  again  within  a  few  seconds.  The  relative  spacing  of 
the  heart  sounds  is  normal.  The  increased  stimuli  do 
not  originate  in  the  heart. 

In  Graves'  disease  the  pulse  is  often  very  rapid — from 
120  upwards.  I  have  counted  it  at  150  or  more  when 
the  patient  has  been  excited,  as  by  a  visit  to  a  physician. 
The  rhythm  is  regular,  and  the  rate  persists  uniformly, 
without  slowing  down  to  near  the  normal  as  with  the 
apprehensive  heart.  The  rapid  action  is  not  caused  by 
abnormal  conditions  in  the  heart. 

Paroxysmal  tachycardia  is  the  term  given  to  a  con- 
dition in  which  the  Avhole  heart,  auricles  and  ventricles, 
jumps  from  about  a  normal  rate  to  one  of  150  or  more, 
and  continues  at  this  rate  for  a  longer  or  shorter  period, 
and  in  spite  of  all  attempts  to  slow  it  down  by  treatment. 
Thus,  I  was  once  listening  to  a  heart  to  make  sure  if  a 
murmur  was  present  when  it  instantaneously  jumped 
from  a  rate  of  80  to  170  a  minute.  It  continued  in 
hospital  for  three  weeks  at  this  pace,  in  spite  of  complete 
rest  in  bed  and  all  drug  treatment,  and  then  stopped  of 
its  own  accord,  and,  as  far  as  I  could  gather,  equally 
suddenly.  I  subsequently  saw  this  case  several  times, 
and  during  the  last  illness,  and  I  thought  it  was  one  of 
mitral  stenosis ;  but  it  proved  to  be  one  of  a  congenital 
septum  in  the  left  auricle,  with  only  a  small  aperture, 
about  half  an  inch  in  diameter,  for  the  blood  to  pass 
through.  There  was  great  enlargement  of  the  liver 
during  the  longer  paroxysms. 

The  paroxysms  of  rapid  action  may  last  from  a  minute 
or  so  to  days  or  months.  The  rate  is  not  materially 
altered  when  the  patient  changes  from  the  erect  to  the 
lying  position  or  vice  versa.  The  stimuli  to  contraction 
arise  from  some  other  j^art  of  the  heart  than  the  sino- 


HEART-BLOCK  101 

auricular  node,  but  there  is  one  beat  of  the  ventricles  to 
every  one  of  the  auricles.  There  is  generally  some 
lesion  in  the  muscle  or  nerve  tissue  of  the  heart. 

Abnormally  slow  pulse. — Many  healthy  people  of  a 
phlegmatic,  stolid  type  have  a  pulse-rate  below  60,  and 
a  similar  slow  beat  is  often  found  in  athletes  used  to 
prolonged  exertion.  I  have  seen  it  in  several  cross- 
country runners,  and  tennis  or  racquet  players,  and 
also  after  acute  illnesses  with  a  high  temperature.  The 
whole  heart,  auricles  as  well  as  ventricles,  partakes  of  the 
abnormal  slowness. 

Bradycardia  is  the  term  applied  to  a  very  slow  pulse 
(40  or  less),  and  its  use  is  best  confined  to  cases  in  which 
there  is  some  pathological  cause,  such  as  heart-block 
(q.v.),  acting  to  produce  the  slow  pulse.  The  beat  of 
the  auricles  is  more  frequent  than  that  of  the  ventricles. 

Heart-block  means  the  interruption  of  the  passage  of 
stimuli  from  the  a.-v.  node  through  the  a.-v.  bundle  to 
the  ventricles,  with  the  result  that  the  ventricle  con- 
tracts only  a  fraction  of  the  number  of  times  stimuli 
from  the  auricles  try  to  pass  to  it.  If  the  block  be  com- 
plete so  that  no  stimuli  pass  from  auricles  to  ventricles, 
the  latter  continue  to  beat  a  rhythm  of  their  own,  which 
is  usually  about  30  per  minute.  In  its  severe  forms  it  is 
due  to  some  disease,  of  sclerotic,  calcareous,  or  gum- 
matous nature,  interrupting  the  integrity  of  the  a.-v. 
bundle,  and  the  number  of  beats  of  the  ventricles  may 
be  reduced  to  9  or  10,  as  in  a  case  under  my  care. 
It  may  be  associated  with  epileptiform  convulsions  in  the 
type  of  disease  known  as  Stokes- Adams  disease. 

Irregular  or  intermittent  pulse — Premature  or 
extrasystole. — In  feeling   a  pulse  it  is  a  very  common 


102  HEART  DISEASE 

occurrence  to  find  that  a  beat  is  missed,  and  simul- 
taneously the  patient  has  an  unusual  sensation  in  the 
chest  as  if  the  heart  stopped  for  a  second  and  then  gave 
an  extra  forcible  beat.  To  this  condition  the  term 
^^  dropped  beat "  is  often  given,  but  it  does  not  correctly 
describe  what  has  happened.  If  the  stethoscope  be 
used  whilst  the  pulse  is  being  felt,  a  very  feeble  beat  of 
the  heart  will  be  heard  to  follow  prematurely  a  normal 
beat,  and  then  a  long  pause  comes  before  another  normal 
beat.  This  early  beat  is  best  called  a  premature  systole, 
as  it  is  not  an  eMra  systole.  It  may  be  too  feeble  to  open 
the  aortic  valve,  when  a  feeble  first  sound  alone  is  heard ; 
or  it  may  be  strong  enough  to  open  the  valve  and 
cause  a  slight  second  sound  but  no  real  pulse-wave. 
Any  accompanying  murmur  will  be  modified  also  in  a 
similar  way.  The  premature  systole  is  brought  about 
by  a  stimulus  arising  in  some  part  of  the  heart  other 
than  the  sino-auricular  node  and  before  its  proper  time. 
The  premature  systole  form  of  cardiac  irregularity  of 
itself,  that  is,  provided  there  is  no  evidence  of  cardiac 
muscle  disease,  namely,  abnormal  frequency  of  heart- 
beat, want  of  diastolic  rest  (tic-tac  rhythm),  valvular 
disease,  muscle  failure,  need  not  alarm,  as  it  is  met  with 
very  frequently  in  apparently  normal  hearts.  A  very 
common  cause  is  a  reflex  action  of  some  functional  dis- 
order of  the  stomach,  especially  flatulence.  Tobacco  is 
probably  another  cause,  acting  directly  on  the  heart  or 
reflexly  through  disturbance  of  the  digestion.  A.  single 
premature  sj^stole,  occurring  occasionally,  is  the  simplest 
form  of  the  condition,  and  the  next  is  a  more  frequent 
repetition  of  the  premature  beat,  varying  to  a  state  in 
which  beats  are  dropped  regularly  every  few  or  more 
(4  to  20)  heart-beats,  and  which  persists  for  years,  or  in 
which  three  or  four  premature  systoles  will  occur  con- 


PREMATURE  SYSTOLE  03 

seciitively  witli  a  flattering  sensation.  Such  a  condition 
often  runs  in  families,  tending  to  be  more  persistent  as 
its  subjects,  often  liable  to  sujDpressed  gout,  grow  older, 
when  there  are  degenerative  changes  in  the  cardiac 
muscle.  By  suppressed  gout  I  mean  a  diathesis  in 
which  the  metabolism  of  food  is  not  carried  to  its  proper 
end-formation  of  urea,  but  stops  in  a  variation  of  the 
sodium  biurate  formation  of  true  articular  gout.  Sup- 
pressed gout  may  lead  to  a  variety  of  ailments,  affecting 
every  system  of  the  body,  which  develop  after  a  period 
of  consumption  of  food  which,  though  not  immoderate, 
is  in  excess  of  the  demand  for  the  body  in  later  adult 
years.  Premature  heart-beats  is  one  of  the  commonest 
of  these  suppressed  gout  manifestations. 

Such  irregularity  generally  passes  off  on  exertion,  and 
may  pass  off  during  an  acute  illness,  or  in  older  people 
may  be  made  worse.  I  have  seen  an  old  patient  of 
seventy-three,  whose  heart  had  been  more  or  less  ir- 
regular for  many  years,  pass  safely  through  an  attack 
of  acute  pneumonia  in  which  there  were  very  few  suc- 
cessive regular  cardiac  cycles  for  three  or  more  days. 
The  heart  seemed  to  roll  over  and  over  in  a  state  of 
delirium  cordis.  With  convalescence  the  usual  degree 
of  irregularity  returned. 

Whilst  cardiac  irregularity  means  nothing  serious 
with  healthy  heart  muscle,  it  is  serious  when  other  signs 
of  muscle  failure,  such  as  breathlessness  on  exertion, 
absence  of  diastolic  rest,  etc.,  are  present. 

Sinus  arrhythmia. — Another  form  of  irregularity  is 
that  arising  from  the  sinus  ;  it  occurs  chiefly  in  young 
people,  and  may  be  produced  by  such  a  physiological 
action  as  swallowing.  Here  diastole  onl}^  is  prolonged, 
systole  being  of  the  normal  length. 

It  has  no  evil  prognostic  significance. 


104  HEART   DISEASE 

AupiculaP  fibrillation  is  tlie  term  given  to  a  condition 
in  which  the  contraction  of  the  auricles  is  so  feeble  and 
indefinite  that  the  muscle  is  thrown  into  a  state  of  fibril- 
lation or  twitching  of  a  very  rapid  nature.  The  auricle 
now  ceases  to  contract  as  a  whole  and  the  a.  wave  dis- 
appears from  a  jugular  tracing.  In  many  if  not  all  of 
the  cases  there  is  some  stretching  of  the  muscle  fibres 
and  dilatation  of  the  cavities  of  the  auricles,  with  also 
some  chronic  inflammatory  process  of  a  fibrotic  nature. 
The  auricular  tissue  becomes  very  excitable  and  re- 
sponds to  stimuli  which  arise  with  very  great  rapidity 
(200  to  300  per  minute)'  from  somewhere  else  than  the 
sino-auricular  node_,  possibly  in  the  auricular  muscle 
itself.  The  conducting  tissue  between  the  auricles  and 
ventricles  in  the  majority  of  cases  is  not  damaged  and 
conducts  a  greatly  increased  number  of  stimuli  to  the 
ventricles.  These  stimuli  are  of  unequal  strength  and 
catch  the  ventricles  at  phases  of  their  cycle  when  they 
cannot  respond  properly  to  any  stimulus.  The  result  is 
usually  increased  frequency  (90  to  150)  of  ventricular 
action  with  extreme  irregularity  of  rhythm  and  of  com- 
pleteness of  contraction.  The  pulse  becomes  quick  and 
very  irregular,  with  scarcely  two  beats  of  a  similar 
nature  following  successively.  The  irregularit}^  of  force 
of  ventricular  contraction  may  only  be  fully  appreciated 
by  using  the  stethoscope  at  the  same  time  that  the  pulse 
is  being  felt.  A  very  irregular  pulse  of  over  1 20  in  rate 
is  almost  certain  to  be  of  auricular  fibrillation  origin. 
Increased  strain  on  the  heart,  such  as  is  caused  by  exer- 
cise, increases  the  number  of  beats  and  also  the  irregu- 
larity of  the  hearths  action. 

Auricular  fibrillation  occurs  most  commonly  in  hearts 
affected  by  rheumatism,  but  it  may  occur  when  there  is 
no  evidence  of  this  disease.     In  the  rheumatic  cases  it  is 


AURICULAR  FIBRILLATION   AND  FLUTTER        105 

very  common  in  mitral  stenosis  and  between  the  ages 
of  twenty  and  sixty,  whilst  in  the  non-rheumatic  cases 
its  incidence  is  later — between  fifty  and  seventy.  The 
quick,  irregular  pulse  of  mitral  stenosis  is  a  typical 
example  of  the  condition.  Although  the  pulse  is  gener- 
ally quick,  it  maybe  slower  and  more  regular;  but  there 
will  always  be  found  some  irregularity  in  the  duration 
of  the  cardiac  cycle  if  careful  measurement  of  the  length 
of  the  arterial  pulse- waves  be  made.  In  a  few  cases 
with  impaired  conduction  through  the  a.-v.  bundle  the 
pulse-rate  may  be  below  normal. 

With  auricular  fibrillation  there  are  generally  present 
some  of  the  usual  signs  of  cardiac  failure  and  back 
pressure  on  the  circulation. 

It  may  persist  for  several  j^ears  in  cases  of  mitral 
stenosis  which  react  to  digitalis  and  are  carefully  treated 
and  dieted ;  the  subjects  of  it  may  be  quite  able  to  keep 
up  aud  about  and  follow  some  clerical  occupation. 

Aupicular  flutter  is  the  term  given  to  a  much  less 
common  condition  which  occurs  chiefly  in  the  later 
years  of  life,  over  fifty,  when  there  is  some  senile  arterio- 
sclerosis and  cardiac  muscle  degeneration  with  or  without 
valvular  disease.  The  auricle  contracts  so  very  rapidly 
(260  to  320  per  minute)  to  stimuli  which  arise — probably 
from  some  single  focus  in  its  own  tissue — that  it  is  in  a 
state  of  flutter.  It  is  almost  always  associated  with 
some  degree  of  heart-block,  so  many  stimuli  being  unable 
to  pass  through  the  a.-v.  bundle,  and  the  ventricle  only 
contracts  one-half,  one-third,  or  a  less  fractional  number 
of  times  of  the  auricular  rate.  It  is  difficult  to  distin- 
guish from  paroxysmal  tachycardia.  The  ventricular 
beating  is  often  regular  in  rhythm  and  completeness  of 
contraction.      Even  when   irregular,   the  irregularity   is 


106  HEART   DISEASE 

more  or  less  regular  in  its  appearance.  The  attacks  may 
last  for  a  few  hours  or  for  months  or  years;  in  the 
former  case  they  may  occur  from  time  to  time  for  several 
years.  In  one  of  Dr.  Lewis's  cases  the  ventricular  rate  was 
160  for  four  years.  If  the  ventricles  take  on  the  full 
auricular  rate  the  attack  is  very  serious,  causing  faintness, 
and  if  it  should  persist  for  more  than  a  few  hours  death 
is  likely  to  ensue.  Firm  pressure  on  the  carotid  artery 
passing  on  to  the  vagus  produces  a  slowing  of  the  pulse. 
Digitalis  often  controls  the  rapidity  of  the  heart-beat 
very  efPectively. 

Further  information  on  the  cardiac  affections  referred 
to  in  this  section  should  be  sought  for  in  Dr.  Thomas 
Lewis\s  valuable  small  work,  ''  Clinical  Disorders  of  the 
Heart-Beat/'  or  in  Sir  James  Mackenzie's  much  larger 
book  on  "  Diseases  of  the  Heart."  I  am  indebted  to 
Dr.  Lewis's  work  for  some  of  the  information  in  this 
section,  especially  in  the  paragraphs  on  Auricular  Fibril- 
lation and  Auricular  Flutter — subjects  which  he  has 
studied  very  closely. 


XII 

TREATMENT   OF   CARDIAC   DISEASE 

The  treatment  of  affections  of  the  heart  centres  chiefly 
round  the  cardiac  muscle,  and  has  for  its  objects : 
(1)  The  prevention  of  weakening  of  the  muscle — that  is, 
of  cardiac  muscle  failure — or  (2),  if  the  cardiac  muscle 
is  already  weakened  or  has  failed,  to  bring  about  com- 
pensation or  prevent  any  further  weakening.  In  other 
words,  treatment  in  heart  affections  may  be  called  for 
(a)  before  muscle  failure,  or  (h)  after  muscle  failure. 

Treatment  of  Cardiac  Affections  before  Muscle 
Failure  develops. 

Many  slight  cases  of  valvular  disease  occur  in  which 
there  is  no  evidence  of  cardiac  muscle  failure.  In  the 
most  favourable  cases  the  heart-rate  is  normal,  there 
is  no  shortness  of  breath,  and  the  patient  leads  a  life 
like  the  average  person.  Slight  murmurs  not  un- 
commonly occur  without  the  patient  knowing  of  their 
existence.     No  treatment  is  called  for  in  these  cases. 

In  the  next  class  of  case  the  lesion  is  a  little  more 
severe,  and,  although  the  heart  may  stand  well  a  quiet 
life,  there  is  no  margin  for  meeting  the  extra  demands 
of  the  muscular  exertion  required  in  periods  of  excite- 
ment, in  going  up  hills  or  stairs  quickly,  or  in  playing 

107 


108  HEART  DISEASE 

games.  In  other  words,  there  is  danger  of  cardiac 
muscle  failure  developing. 

The  treatment  in  these  borderland  cases  must  be 
directed  to  helping  the  heart  muscle  to  keep  up  with  its 
work.  It  must  be  saved  from  the  influence  of  adverse 
forces  acting  directly  on  it,  chiefly  muscular  over- 
exertion, and  indirectly  or  reflexly  from  the  nervous 
and  alimentary  systems. 

Mental  excitement,  which  tends  to  quicken  the  action 
of  shaky  hearts,  must  be  avoided,  and  a  proper  amount 
of  sleep  should  be  secured. 

Diet. — In  the  alimentary  system  the  diet  should  be  so 
ordered  as  to  avoid  the  development  of  flatulence  in  the 
stomach  which  tends  to  excite  an  abnormal  heart.  This 
is  most  surely  brought  about  b}'  the  avoidance  of  too 
much  starch  and  sugar  food,  and  especially  by  not 
taking  these  foods  with  the  heavy  meals  of  the  day  in 
which  flesh  foods  are  consumed.  It  is  surprising  what 
a  difference  the  dyspeptic  feels  when  he  takes  a  meal 
consisting  only  of  fish  or  meat,  green  vegetables,  toast, 
and  even  potatoes,  as  compared  with  when  he  takes  in 
addition  even  small  amounts  of  "  sweets  "  in  the  form  of 
milk  pudding,  or  any  other  pudding  made  with  starch 
and  sugar.  The  discomfort  of  the  second  type  of  meal 
arises  partly  from  the  greater  amount  consumed  at  it, 
and  partly  from  the  flatulence  which  such  a  proteid  and 
starch  meal  produces.  The  carbohydrates  and  fats 
should  be  taken  at  breakfast  in  the  form  of  porridge, 
toast,  brown  bread,  butter,  fat  bacon,  milk,  or  cream. 
Tea,  coffee,  or  cocoa  with  mixed  meals  comprising  partly 
flesh  foods  are  very  liable  to  cause  flatulence. 

The  hoiveh  should  he  kept  regular,  using,  if  necessar}"-, 
some  simple   non-irritant   aperient,   two  of  the   best  of 


TREATMENT  OF  MUSCLE  FAILURE  109 

which  are  cascara,  or  the  pill  of  colocynth  and  hyoscy- 
amus  in  two  and  a  half  grain  or  larger  doses.  Purga- 
tion must  be  avoided,  and  saline  aperients  often  cause 
considerable  gastro-intestinal  disturbance. 

Exercise  should  be  encouraged,  but  this  must  be  well 
within  the  capacity  of  the  heart.  The  pulse-rate  should 
not  be  raised  too  high  by  it,  and  should  subside  to  the 
normal  rate  within  reasonable  time  after  resting.  Short- 
ness of  breath  should  especially  be  avoided.  Too  much 
is  being  done  if  the  patient  cannot  take  his  food  and 
sleep  properly.  Golf  is  a  useful  form  of  exercise  if  taken 
leisurely  and  in  moderate  amount,  but  not  if  played  too 
vigorously  or  too  long. 

Medicinal  treatment  in  these  cases  is  directed 
towards  keeping  the  heart  from  getting  overstrained, 
and  should  be  of  a  general  nature  calculated  to  keep  the 
whole  body  in  as  healthy  a  condition  as  possible.  The 
digestion  should  be  helped  if  necessary  by  stomachic 
mixtures,  tincture  of  nux  vomica,  or  strychnine,  being 
specially  useful ;  and  the  blood  should  not  be  allowed  to 
become  anaemic,  arsenic  and  iron  preparations  being 
used  for  this  purpose. 

Treatment  of  Cardiac  Muscle  Failure. 

Rest  in  bed. — As  the  muscle  failure  is  the  result  of 
overwork,  the  first  indication  for  its  treatment  is  rest, 
and  the  only  way  to  secure  this  properly  is  to  keep  the 
patient  in  bed  altogether,  even  using  the  bed-pan  for  the 
bowels.  It  is  no  use  letting  the  patient  get  up  and  lie 
on  the  couch.  The  exertion  of  dressing  is  considerable, 
and  any  exertion  increases  the  heart-rate  considerably 
in  muscle  failure.  The  saving  of  the  work  of  the 
heart  which  complete  rest  in  bed,  as  compared  with  the 


110  HEART   DISEASE 

"  up  and  about  ^'  condition,  insures,  can  be  seen  by  a 
simple  arithmetical  sum.  There  is  frequently  a  difference 
of  20  and  30  beats  per  minute  between  the  two  condi- 
tions in  cardiac  debility — that  is,  1,200  to  1,800  an  hour, 
or  14,000  to  20,000  per  twelve  hours.  To  save  the  heart 
this  work  means  good  progress  on  the  upward  journey. 
It  is  astonishing  to  those  seeing  it  for  the  first  time  how 
complete  rest  in  bed,  without  any  drugs,  in  cases  of 
general  oedema  from  muscle  failure,  especially  if  due  to 
alcoholic  poisoning,  will  lead  to  elimination  of  the  fluid 
by  spontaneous  diuresis.  It  is  not  uncommon  to  see 
patients,  who  on  admission  pass  only  20  ounces  of  urine 
a  day,  begin,  after  three  or  five  or  so  days  in  bed,  to 
pass  50,  100,  150,  or  180  ounces  per  day  with  almost 
visible  shrinking  to  normal  bulk. 

Diet. — The  diet  in  cases  of  cardiac  muscle  failure 
must  be  on  the  same  lines  as  that  ordered  in  the  earlier 
stages  of  heart  affections.  It  suits  the  patients  best  to 
be  kept  more  rigidly  to  flesh  foods.  The  lighter  forms 
of  flesh  foods  are  the  best.  No  duck,  goose,  salmon, 
pork,  veal,  or  high  game,  should  be  allowed.  Made-up 
dishes  with  rich  gravy,  and  sauces  or  soups  thickened 
with  flour  and  burnt  fats  are  all  very  productive  of 
flatulence. 

It  is  also  important  to  keep  the  diet  as  free  from  fluid 
as  possible,  so  as  to  try  and  promote  the  absorption  of  the 
excess  of  fluid  which  tends  to  remain  in  the  tissues. 

The  bowels  must  be  kept  acting  daily,  without  purging, 
but  with  fluid  evacuations  if  there  is  oedema  present. 
When  the  liver  is  enlarged,  some  blue  pill  is  useful.  It 
can  be  given  in  the  form  of  Pil.  diuretica  (Guy^s  pill) 
three  times  daily,  or  else  in  larger  single  doses,  3  grains 
at  night  twice  or  three  times  a  week.  It  should  be 
followed  in  the  morning  by  a  saline  aperient. 


TREATMENT  OF  MU8CLE  FAILURE  111 

Sleep. — One  of  the  most  distressing  results  of  severe 
cardiac  muscle  failure,  especially  with  much  enlarge- 
ment of  the  heart,  is  inability  to  sleep  restfuUy,  or  even 
to  sleep  at  all.  This  is  due  in  great  part  to  the  tumul- 
tuous contraction  of  the  big  heart,  and,  with  aortic  in- 
competence, to  throbbing  of  the  carotid  arteries  as  well. 
These  movements  are  so  marked  that  they  constantly 
disturb  the  patient,  and  even  if  sleep  comes  from  ex- 
haustion it  is  not  restful  and  sooner  rather  than  later 
the  patient  wakes  up  in  a  fright  with  a  sense  of  suffo- 
cation. There  is  no  chance  of  sleeping  in  any  but  the 
sitting  position,  and  not  uncommonly  only  when  the 
trunk  and  head  incline  forward.  In  the  worst  forms 
bed  is  impossible,  and  an  armchair  the  only  resort. 

In  milder  cases  a  glass  of  hot  whisky  and  water  may 
help,  and  the  addition  of  a  drachm  of  ethyl  nitrite  when 
there  is  any  high  tension  will  give  some  relief.  Chloral 
and  bromide  are  useful  in  the  more  advanced  stage,  and 
the  former  drug  can  be  given  without  any  fear,  as  it  is 
not  really  depressant  to  the  heart.  Even  if  chloral  were 
depressant,  no  harm  would  be  done  to  a  vigorously  over- 
acting heart.  Chloralamide  may  also  be  tried ;  par- 
aldehyde is  useful,  but  it  is  objectionable  to  take. 
Unfortunately,  very  often  none  of  these  drugs  help 
matters,  and  then  morphia  must  be  used.  When  given 
hypodermically  in  quarter-grain  doses  with  y^jj  grain 
of  atropine  some  restful  sleep  may  be  obtained.  Alcohol 
may  help  towards  securing  sleep. 

Drug's. — The  medicinal  like  the  general  treatment  of 
heart  failure  is  primarily  directed  towards  strengthening 
the  muscle  and  removing  the  oedema,  and  the  groups  of 
drugs  used  for  these  purposes,  with  their  most  useful 
members,  are — 


112  HKART   DISEASE 

1.  Drugs  acting  on  the  cardiac  muscle  —  digitalis, 
strophanthus,  and  caffein  citrate. 

2.  Drugs  acting  as  vessel  dilators — the  nitrite  group, 
especially  sodium  and  ethyl  nitrites. 

3.  Diuretics — digitalis,  caffein  citrate,  theobromine 
iand  sodium  salicylate,  theocin  sodium  acetate. 

Drugs  acting  on  the  Cardiac  Muscle. 

Dig^italis  is  the  most  useful  drug  in  the  treatment  of 
heart  disease.  It  slows  the  heart  by  prolonging  diastole, 
and  it  also  tends  to  raise  the  blood-pressure.  Its  indica- 
tion is  cardiac  muscle  failure,  and  not  any  special 
valvular  disease.  It  may  also  act  well  in  muscle  failure 
from  degeneration,  fatty  or  fibroid,  but  its  use  in  these 
conditions  must  be  carefully  watched. 

If  digitalis  will  do  good  it  can  almost  always  be 
tolerated,  but  sometimes  it  disagrees  from  personal 
intolerance  of  the  drug  before  an^^  question  of  over- 
dosage arises,  and  causes  nausea,  vomiting,  and  looseness 
of  the  bowels.  True  overdosage  may  cause  cardiac 
irregularity  or  coupling  of  the  heart-beats,  which  will 
return  to  normal  after  discontinuance  of  the  drug  and 
treatment  in  bed  alone. 

When  digitalis  has  been  given  for  some  time  the  urine 
often  becomes  diminished  in  amount  before  nausea 
appears — a  warning  to  stop  its  use. 

A  watery  extract,  especially  the  freshly  prepared  infu- 
sion (one  to  two  drachms  three  times  daily)  is  the  best ; 
but  it  is  very  convenient  to  prescribe  it  in  granule  form 
(_i_j.  milligramme  of  digitalin),  people  with  mitral  disease 
and  secondary  muscle  failure, especially,  sometimes  taking 
one  every  morning  with  great  advantage  for  years.  If 
it  is  desired  to  push  the  drug  a  granule  may  be  given 


DIGITALIS   AND   STROPHANTHUS  113 

twice  or  three  times  daily.     The  tincture  in  ten  to  fifteen 
minim  doses  three  times  daily  is  also  useful. 

Digitalis  acts  best  in  cardiac  muscle  failure  and 
dilatation  of  the  ventricles  from  overwork  in  which 
there  are  signs  of  back  pressure  or  oedema  so  often 
associated  with  mitral  disease  or  alcoholism.  Whilst  it 
often  acts  well  in  cases  with  a  quick  irregular  pulse 
associated  with  auricular  fibrillation  and  with  some 
oedema,  it  is  impossible  to  tell  definitely  whether  it  will 
act  or  not.  No  instruments  can  supply  us  with  this 
knowledge.  It  is  also  useful  in  aortic  incompetence 
with  ventricular  dilatation,  provided  the  pulse  is  above 
80  when  the  patient  is  in  bed. 

Cases  of  valvular  disease  in  which  the  heart  is  beating 
slowly  (70  to  80)  and  regularly,  and  there  is  no  shortness 
of  breath,  do  not  need  digitalis.  A  simple  general  tonic 
like  nux  vomica  is  enough,  with  a  healthy  mode  of  life 
and  a  diet  which  will  avert  flatulence. 

Digitalis  must  be  used  with  caution  in  hearts  which 
give  evidence  of  senile  decay,  fatty  degeneration,  or 
cardiosclerosis,  but  when  so  used  is  often  invaluable. 
If  it  is  desired  to  use  it  with  high  tension,  which  it 
increases,  some  vessel  dilator  should  be  given  at  the 
same  time.  An  excellent  prescription  for  high  tension 
is  a  grain  and  a  half  each  of  sodium  and  potassium 
iodides,  a  quarter  to  half  a  grain  of  sodium  nitrite  and 
water  to  half  an  ounce  three  times  a  day. 

If  digitalis  does  not  act  on  the  cardiac  muscle  other 
drugs,  in  my  experience,  are  unlikely  to  do  so,  but 
strophanthus  or  caffein  citrate  may  be  tried. 

Strophanthus  acts  on  the  heart  like  digitalis,  but  it 
does  not  raise  the  blood-pressure.  It  may  be  useful; 
therefore,  if  there  is  a  tendency  to  high  tension,  which 
digitalis  will  emphasize,  and  also  in  cases  which  cannot 

8 


114  HEART   DISEASE 

tolerate  digitalis.     The  new  tincture  is  much  stronger 
than  the  old  one  and  the  dose  is  2  to  5  minims. 

CafFein  citrate  stimulates  the  heart  by  increasing  the 
frequency  of  its  beat  and  decreasing  diastole.  Its 
diuretic  effect  helps.  But  there  are  only  a  few  cases 
which  will  react  to  it  and  not  to  digitalis  and  strophan- 
thus.  Two  to  three  grains  in  water  thrice  daily  is  a 
sufficient  dose. 

Strychnine  or  nux  vomica  even  in  large  doses,  in  my 
opinion,  is  not  of  any  real  value  as  a  heart  muscle  stimu- 
lant and  restorative.  These  drugs  act  as  tonics — that  is, 
they  tend  to  stimulate  the  stomach  and  to  enable  it  to 
start  the  processes  of  digestion  of  food  better.  With 
improved  digestion  there  is  improved  absorption  of  food 
and  consequent  improvement  of  the  whole  system,  in- 
cluding the  heart. 

Vessel  Dilators. 

The  nitrites  are  most  useful  drugs  whenever  high 
tension  is  present,  as  indicated  by  the  condition  of  the 
radial  pulse  or  by  dyspnoea  of  the  asthmatic  or 
paroxysmal  type.  For  prolonged  treatment  of  high 
tension  a  mixture  containing  sodium  nitrite  (one  quarter 
to  half  a  gi'ain),  with  small  doses  of  iodides  of  potash 
and  soda  (of  each  one  and  a  half  grains),  in  half  an  ounce 
of  water,  three  times  a  day  is  most  valuable.  For  more 
rapid  relief  the  solution  of  ethyl  nitrite  is  very  effective. 
Many  heart  cases  are  liable  to  attacks  of  dyspnoea  at 
night  and  these  are  relieved  by  a  teaspoonful  of  ethyl 
nitrite  solution  in  a  little  water,  followed  immediately  by 
a  tablespoonful  of  whisky  in  hot  water.  The  ethyl 
nitrite  is  very  volatile,  must  be  kept  in  well-stoppered 
bottles,  and  must  not  be  given  in  hot  water. 


TREATMENT  115 


Diuretics. 


If  digitalis  fails  to  remove  dropsy,  and  there  is  no 
nephritis,  theobromine  and  sodium  salicylate  (gr.  x.  t.d.s. 
for  an  adult)  often  will.  Theocin  sodium  acetate 
(gr.  V.  t.d.s.)  is  also  often  useful. 

Complete  rest  in  bed  on  light  diet  is  one  of  the  best 
diuretics,  especially  in  alcoholic  cardiac  muscle  failure 
with  general  oodema.  After  four  or  five  days  the  urinary 
output  begins  to  go  up  rapidly,  with  gradual  decrease  in 
the  oedema.  Guy^s  pill,  or  Pil.  diuretica,  consisting  of 
a  grain  each  of  powdered  digitalis  leaves,  powdered 
"squill,  blue  pill,  and  extract  of  hyoscyamus,  given  three 
times  a  day,  is  a  most  useful  method  of  treating  these 
cases.  The  diuresis  that  follows  its  administration  is 
often  very  marked. 

Treatment  of  Special  Forms  of  Heart  Disease. 

Mitral  disease. — Mitral  stenosis  with  more  or  less 
incompetence  is  the  most  common  form  of  heart  disease 
in  adult  life.  Its  presence  may  not  be  suspected  and 
may  only  be  recognized  when  an  examination  is  made 
for  some  purpose  not  connected  with  a  suspicion  of  any 
heart  trouble,  as,  for  instance,  a  life  insurance  proposal. 
Such  people  lead  an  active  life  like  their  fellows  with 
perfectly  sound  hearts.  In  these  cases  the  leakage  is 
small  and  has  no  bad  effects. 

Many  other  cases  in  which  there  is  evidence  of  cardiac 
weakness,  quickened  heart-rate,  breathlessness,  especially 
on  exertion,  but  without  oedema,  can  get  about  quite 
comfortably  for  years  with  the  help  of  digitalis ;  when 
the  drug  acts  it  acts  well,  and  a  granule  of  ^\-ij  grain  of 
Nativelle^s  digit alin,  given  daily  at  breakfast- time,  or 


116  HEART   DISEASE 

one  of  7;  Jo  grain  given  three  times  daily,  has  kept  people 
on  their  legs  for  years.  Such  patients  must,  however, 
rest  as  much  as  possible  in  the  day-time. 

The  drug  can  be  used  as  long  as  it  does  not  cause 
nausea,  or  does  not  slow  the  pulse  below  70.  With 
oedema  present  digitalis  still  acts  well,  but  rest  in  bed 
is  necessary  in  addition. 

The  quick,  irregular  heart  of  auricular  fibrillation  met 
with  in  these  cases  is  often  considerably  steadied  by  this 
treatment,  especially  if  oedema  be  present,  but  if  there 
are  no  back-pressure  symptoms  it  is  often  very  disap- 
pointing to  find  that  no  treatment  whatever  improves 
the  condition.  The  only  thing  to  be  done  is  to  give 
cardiac  and  general  sedatives,  especially  the  bromides. 
These  are  as  difficult  cases  to  deal  with  as  any  in  cardiac 
disease. 

All  patients  taking  digitalis  must  be  watched  carefully, 
as  the  drug  is  cumulative  in  its  action,  and  if  given  for 
too  long  a  time  may  slow  the  pulse  too  much,  and  produce 
coupling  of  the  beats  and  gastro-intestinal  symptoms. 

Aortic  disease. — This  disease  does  not  contra-indicate 
digitalis  if  there  is  any  muscle  failure.  It  can  be  safely 
given,  and  should  be  given,  even  in  extreme  regurgita- 
tion, provided  the  pulse-rate  does  not  slow  down 
below  80. 

Alcoholic  heart  failure,  with  oedema,  and  with  or 
without  valvular  incompetence,  does  splendidly  on  the 
rest  in  bed  alone,  a  diuresis  coming  on  which  clears  off 
the  oedema.  Digitalis,  especially  the  infusion,  acts  at 
its  best  in  these  cases,  and  soon  strengthens  the  heart 
muscle  and  hastens  the  diuresis.  Rest  in  bed  is,  how- 
ever, also  essential  for  this  action  of  the  drug. 


TREATMENT  OF  ANGINA   PECTORIS  117 

Angfina  pectoris. — During  an  attack  one  of  the  vessel 
dilators,  the  nitrites,  must  be  used.  In  the  milder  cases 
they  will  relieve  the  pain.  Many  patients  carry  amyl 
nitrite  capsules  in  their  pockets  and  inhale  the  drug 
during  the  attack.  In  less  severe  cases  a  trinitrin  tablet 
is  carried,  and  taken  if  there  are  threatenings  of  pain. 
In  the  most  severe  cases  it  is  necessary  to  give  a  hypo- 
dermic injection  of  morphia. 

Between  the  attacks  treatment  is  directed  to  removing 
calcareous  deposits  from  the  arteries  of  the  heart  and 
to  preventing  any  further  deposition  of  them.  Phos- 
phoric acid  is  very  useful  for  this  ;  twenty  minims  of 
the  dilute  acid  with  infusion  of  calumba  and  spirits  of 
chloroform,  given  three  times  a  day  after  food  for  some 
weeks,  has  been  followed  by  great  freedom  from  attacks. 

If  the  disease  occurs  in  people  below  forty-five  or  fifty, 
syphilis  must  be  suspected.  The  Wassermann  reaction 
should  be  done,  and,  if  positive,  treatment  with  mercury 
inunction  and  iodide  of  potash  instituted;  salvarsan  is 
dangerous  in  these  cases. 

When  there  is  evidence  of  cardiac  muscle  failure  with 
dilatation  of  the  heart  this  must  be  treated  carefully  by 
approved  measures.  The  question  of  exercise  in  people 
liable  to  angina  pectoris  is  a  very  important  matter. 
Only  that  which  cannot  throw  a  strain  on  the  heart 
should  be  allowed,  and  golf  is  not  such  an  exercise. 


INDEX 


Alcoholic  heart,  treatment,  116 
Anatomy,  1,  2 
Angina  pectoris,  96 

,  treatment,  117 

Anxiety,  20 

Aortic  disease,  face  in,  19 

,  prognosis,  86 

,  treatment,  116 

Aortic  murmurs,  66,  83 

,  crescendo,  86 

,  diastolic,  85 

— — ,  see-saw,  86 

,  systolic,  83 

Aortic  valve,  condition  of,  85 
Apex  -  beat,     displacement     of, 
27 

in  disease,  23 

,  localization,  27,  28 

,  normal,  23 

Apprehensive  heart,  99 

Arterial  pulse,  8 

,  visible,  20 

Artery  wall,  condition  of,  14 

Auricular  fibrillation,  104 

flutter,  105 

Auriculo-ventricular  valves,  dila- 
tation, 57 

,  stenosis,  55 

Auscultation,  27 

A.-v.  bundle,  4 

A.-v.  node,  4 

Blood  pressure,  changes  in,  35, 

42 
Bradycardia,  101 
Breath,  shortness  of,  6 
Bruit  de  diable,  90 


Caffein  citrate,  114 
Cardiac  dilatation  without  mur- 
mur, 57 
Cardiac  dulness,  26,  27 
Cardiac  impulse,  absent,  23 

,  inspection,  21 

,  palpation,  22 

Cardio-pleural  sounds,  92 
Cardio-pulmonary  sounds,  92 
Cardio-respiratory  sounds,  92 
Complaints,  patients',  6 
Conduction  of  murmurs,  68 
Congenital  heart  disease,  19 
Cough,  8 
Crescendo  murmur,  59 

,  aortic,  85 

,  causation,  60 

,  location,  79 

,  mitral,  78 

,  prognosis,  82 

,  rhythm,  60 

,  semilunar  valve,  61 

,  time,  82 

,  with  other  murmurs,  80 

Cyanosis,  19 

Diet,  108,  110 
DigitaUs,  112 
Dropsy,  8 
Dyspnoea,  6 

Electrocardiogram,  98 
Endocarditis,  malignant,  93 

,  septic,  93 

,  ulcerative,  93 

Exercise,  109 
Exocardial  sounds,  91 


118 


INDEX 


119 


Fluid  veins,  51 
Friction,  pericardial,  24 

General  signs  of  heart  disease,  18 

Haemic  murmurs,  54 

,  cardiac,  89 

,  vascular,  90 

Haemorrhage,  7 

Heart  -  beat,   nervous    mechan- 
ism, 3 
Heart-block,  101 
Heart  dulness,  limits,  25 
Heart  rhythm,  irregularities,  98 
Heart  sounds,  bruit  de  galop,  46 

,  cantering  rhythm,  46 

,  embry ©cardial  rhvthm,  46 

,  first,  29 

,  rhythm,  45 

,  second,  41 

Inspection,  general,  of  neck,  17 
,  of  praecordia,  17 

Jaundice,  20 

Medicinal  treatment,  109 
Mitral  disease  treatment,  115 
Mitral  murmurs,  diastolic,  77,  78 

,  systolic,  72,  76 

Mitral  stenosis,  face  in,  18 
Mitral  valve,  66 

,  condition  of,  76 

Murmurs,  and  heart  sounds,  61 

,  area  of  audibility,  65 

,  causation,  48 

,  conduction,  68 

,  physical  causes,  51 

,  timing,  48 

,  transmission,  68 

Murmurs,  aortic,  69,  83 

,  crescendo,  70,  78 

,  haemic,  54 

,  mitral,  70,  72 

,  posture,  87 

,  pulmonary,  69,  87 

,  tricuspid,  68,  82 

Muscle,  cardiac,  importance  of 
condition  of,  53 


Neck,  inspection  of,  20 
Nervous  mechanism,  3 
Nipple,  line,  2 

,  position  of,  2 

Nitrites,  114 

Node,  auriculo-ventricular,  4 

,  sino-auricular,  3 

Nodules,  rheumatic,  75 

Obstruction,  valvular,  50 

Pain,  7 
Palpation,  22 
Palpitation,  6 
Percussion,  methods,  24 
Pericardial  adhesion,  95 

effusion,  94 

friction,  24,  91 

sounds,  91 

Pericarditis,  94 

purulent,  95 

serous,  94 

Pericardium,  adherent,  95 
Polyuria,  nocturnal,  13 
Posture,     effect     on     murmurs, 

67 
Posture  murmur,  87 
Praecordia,  bulging,  22 
Premature  systole,  101 
Pulmonary  valve,  67 
Pulmonary  murmurs,  87 

prognosis,  88 

Pulse,  abnormalities,  10 

,  arterial,  8 

,  feeling  of,  10 

,  intermittent,  101 

,  irregular,  101 

,  jugular,  15,  16 

,  radial,  10 

,  rate,  10 

,  slow,  101 

,  tension,  13 

,  varieties,  12 

,  venous,  15 

Rest  in  bed,  109 
Retraction  of  interspaces,  22 
Rheumatism  in  childhood,  74 


120 


INDEX 


Rheumatism  in  childhood,  his- 
tory of,  74 

,  nodules,  75 

Routine  examination,  6 

Second  sound,  causation,  40 

,  characteristics,  41 

,  modifications,  33 

,  reduplication,  44 

,  variations,  42 

Semilunar  valves,  58 

,  anatomy,  37 

,  mechanism,  37 

Sinus  arrhythmia,  103 
Sounds,  absence,  62 
Stenosis,  50,  56 

,    absolute    or    actual,    50, 

52,  56 
-,  relative,  50,  52 


Stethoscope,  use  of,  28 
Strophanthus,  113 
Strychnine,  114 
Surface  lines,  3 
Systole,  premature,  101 


Tachycardia,  99 

,  paroxysmal,  100 

Tension,  high,  13 

,  low,  14 

Thrills,  23,  54 
Tic-tac  rhythm,  45 
Tricuspid  murmurs,  82,  83 

,  prognosis,  83 

Tricuspid  valve,  66 
Treatment,  107 

Valves,  auriculo-ventricular,  29 

,  dilatation,  63 

,  incompetence,  50 

,  mobility,      influence 


on 


sounds,  64 
— ,  obstruction,  50,  56 
— ,  semilunar,  39 
— ,  situation,  65 
— ,  stenosis,  50 
— ,  ulceration,  58 
-,  vegetations  on,  56 


Veins,  condition  of,  20 
Vibration  of  valve  curtains,  53 


H.    K.    LEWIS  &  CO.,  LTD.,   13G  COWER  STKKtT,    LOtiDOS,    W.C. 


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